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125 gesichtete, geschützte Fragmente: Plagiat

[1.] Jm/Fragment 092 12 - Diskussion
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Resilience has been described as an individual’s capacity for maintenance, recovery or improvement in mental health following life challenges (Ryff et al., 1998), successful adaptation following exposure to stressful life events (Werner, 1989), and an individual’s capacity for transformation and change (Lifton, 1993).

Lifton, R.J. (1993). The protean self: Human resilience in an age of transformation. New York: Basic Books.

Ryff, C.D., Singer, B., Dienberg Love, G., & Essex, M.J. (1998). Resilience in adulthood and later life. In J. Lomaranz (Ed.), Handbook of aging and mental health: An integrative approach (pp. 69-96). New York: Plenum Press.

Werner, E.E. (1993). Risk, resilience, and recovery: Perspectives from the Kauai longitudinal study. Development and Psychopathology, 5, 503-515.

Resilience has been described as an individual’s capacity for maintenance, recovery or improvement in mental health following life challenges (Ryff, Singer, Dienberg Love, & Essex, 1998), successful adaptation following exposure to stressful life events (Werner, 1989), and an individual’s capacity for transformation and change (Lifton, 1993)

Lifton, R. J. (1993). The protean self: Human resilience in an age of transformation. New York: Basic Books

Ryff, C. D., Singer, B., Dienberg Love, G., & Essex, M. J. (1998). Resilience in adulthood and later life. In J. Lomaranz (Ed.), Handbook of aging and mental health: An integrative approach (pp. 69-96). New York: Plenum Press.

Werner, E. E. (1993). Risk, resilience, and recovery: Perspectives from the Kauai longitudinal study. Development and Psychopathology, 5, 503-515.

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[2.] Jm/Fragment 201 16 - Diskussion
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Fragment, Gesichtet, Jm, SMWFragment, Schutzlevel sysop, Verschleierung, Wikipedia Anterior cingulate cortex 2007

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Interestingly, this region is associated with many functions that require conscious experience by the viewer. For example, higher anterior cingulate cortex activation levels were found for more emotionally aware female participants when shown short ‘emotional’ video clips (Lane et al., 1998). Better emotional awareness is associated with improved recognition of emotional cues or targets which is reflected by anterior cingluate activation.

Lane, R.D., Reiman, E.M., Axelrod, B., Yun, L.S., Holmes, A., & Schwartz, G.E. (1998). Neural correlates of levels of emotional awareness. Evidence of an interaction between emotion and attention in the anterior cingulate cortex. Journal of Cognitive Neuroscience, 10(4), 525-535.

The ACC area in the brain is associated with many functions that require conscious experience by the viewer. Higher ACC activation levels were found for more emotionally aware female participants when shown short ‘emotional’ video clips (Lane et al., 1998). Better emotional awareness is associated with improved recognition of emotional cues or targets which is reflected by ACC activation.

Lane, R.D., Reiman, E.M., Axelrod, B., Yun, L., Holmes, A., & Schwartz, G.E. (1998). Neural correlates of levels of emotional awareness: Evidence of an interaction between emotion and attention in the anterior cingulate cortex. Journal of Cognitive Neuroscience, 10(4), 525-535.

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[3.] Jm/Fragment 160 09 - Diskussion
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Many ERP studies of recognition memory have been interpreted within dual-process frameworks that differentiate between familiarity and recollection (Brainerd et al., 1995; Hintzman & Curran, 1994; Jacoby, 1991). Though details differ between theories, familiarity is generally considered to reflect an assessment of the global similarity between study and test items (Hintzman, 1988; Gillund & Shiffrin, 1984), whereas recollection allows for the retrieval of detailed information concerning study items such as physical attributes or associative/contextual/source information. Within the context of such theories, studies indicate that an ERP old/new effect occurring between 400ms and 800ms is related to putative memory retrieval processes (Johnson, 1995; Rugg, 1995).

Brainerd, C. J., Reyna, V.F., & Kneer, R. (1995). False-recognition reversal: When similarity is distinctive. Journal of Memory and Language, 34, 157–185.

Gillund, G., & Shiffrin, R.M. (1984). A retrieval model for both recognition and recall. Psychological Review, 91, 1–67.

Hintzman, D.L. & Curran, T. (1994). Retrieval dynamics of recognition and frequency judgments: evidence for separate mechanisms of familiarity and recall. Journal of Memory and Language, 33, 1-18.

Hintzman, D. (1988). Judgments of frequency and recognition memory in a multiple trace memory model. Psychological Review, 95, 528–551.

Jacoby, L.L. (1991). A process dissociation framework: separating automatic from intentional uses of memory. Journal of Memory and Language, 30, 513–541.

Johnson R Jr (1995). Event-related insights into the neurobiology of memory systems. In F. Butler and J. Grafman (Eds.), Handbook of neuropsychology (vol 10, pp 135–163). Amsterdam: Elsevier.

Rugg, M.D. (1995). ERP studies of memory. In M.D. Rugg and M.G.H. Coles (Eds.), Electrophysiology of mind (pp. 132- 170). Oxford: Oxford University Press.

Many ERP studies of recognition memory have been interpreted within dual-process frameworks that differentiate between familiarity and recollection [8, 19, 23, 31]. Though details differ between theories, familiarity is generally thought to reflect an assessment of the global similarity between studied and tested items [16, 17], whereas recollection enables the retrieval of detailed information. Within the context of such theories, recent studies indicate that an ERP old/new effect occurring between 400 and 800 ms (subsequently denoted the 'P600 old/new effect' (following [44]) is related to recollection [2, 35, 36, 43, 49, 51, 58, 59, 61].

[2] Allan K, Wilding EL, Rugg MD. Electrophysiological evidence for dissociable processes contributing to recollection. Acta Psychologica 1998;98:231-52.

[8] Brainerd CJ, Reyna VF, Kneer R. False-recognition reversal: When similarity is distinctive. Journal of Memory and Language 1995;34:157-85.

[16] Gillund G, Shiffrin RM. A retrieval model for both recognition and recall. Psychological Review 1984;91:1-67.

[17] Hintzman DL. Judgments of frequency and recognition memory in a multiple-trace memory model. Psychological Review 1988;95:528-51.

[19] Hintzman DL, Curran T. Retrieval dynamics of recognition and frequency judgments: Evidence for separate processes of familiarity and recall. Journal of Memory and Language 1994;33:1- 18.

[23] Jacoby LL. A process dissociation framework: separating automatic from intentional uses of memory. Journal of Memory and Language 1991;30:513-41.

[31] Mandler G. Recognizing: The judgment of previous occurrence. Psychological Review 1980;87:252-71.

[35] Paller KA, Kutas M. Brain potentials during memory retrieval provide neurophysiological support of the distinction between conscious recollection and priming. Journal of Cognitive Neuroscience 1992;4:375-91.

[36] Paller KA, Kutas M, McIsaac HK. Monitoring conscious recollection via the electrical activity of the brain. Psychological Science 1995;6:107-11.

[43] Rugg MD, Cox CJC, Doyle MC, Wells T. Event-related potentials and the recollection of low and high frequency words. Neuropsychologia 1995;33:471-84.

[44] Rugg MD, Doyle MC. Event-related potentials and recognition memory for low- and high-frequency words. Journal of Cognitive Neuroscience 1992;5:69-79.

[49] Smith ME. Neurophysiological manifestations of recollective experience during recognition memory judgments. Journal of Cognitive Neuroscience 1993;5:1-13.

[51] Smith ME, Halgren E. Dissociation of recognition memory components following temporal lobe lesions. Journal of Experimental Psychology: Learning, Memory, and Cognition 1989;15:50-60.

[58] Wilding EL, Doyle MC, Rugg MD. Recognition memory with and without retrieval of context: an event-related potential study. Neuropsychologia l99S;33:743-67.

[59] Wilding EL, Rugg MD. An event-related potential study of recognition memory with and without retrieval of source. Brain l996;ll9:889-90S.

[61] Wilding EL, Rugg MD. An event-related potential study of recognition memory for words spoken aloud or heard. Neuropsychologia l997;35:ll85-95.

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[4.] Jm/Fragment 161 18 - Diskussion
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Second, the parietal old/new effect is sensitive to variables thought to affect recollection more than familiarity such as depth of processing (Rugg, Allan & Birch, 2000; Rugg et al., 1998; Paller, Kutas & McIsaac, 1995; Pallar & Kutas, 1992). Third, when participants are asked to introspectively differentiate words specifically ‘remembered’ from those merely ‘known’ to be old, larger parietal old/new effects are associated with ‘remembering’ than ‘knowing’ (Düzel et al., 1997; Rugg, Schoerscheidt & Mark, 1998; Smith, 1993; but also see Spencer, Vila Abad & Donchin, 2000).

Düzel, E., Yonelinas, A.P., Mangun, G.R., Heinze, H.J., & Tulving, E. (1997). Event-related brain potential correlates of two states of conscious awareness in memory. Proceedings of the National Academy of Sciences 94, 5973-5978.

Paller, K. A. & Kutas, M. (1992). Brain potentials during memory retrieval provide neurophysiological support for the distinction between conscious recollection and priming. Journal of Cognitive Neuroscience, 4, 375-391.

Paller, K. A., Kutas, M., & McIsaac, H. (1995). Monitoring conscious recollection via the electrical activity of the brain. Psychological Science, 6, 107-111.

Rugg, M.D., Allan, K., & Birch, C.S. (2000). Electrophysiological evidence for the modulation of retrieval orientation by depth of study processing. Journal of Cognitive Neuroscience, 12(4), 664- 678.

Rugg, M.D., Mark, R.E., Walla, P., Schloerscheidt, A.M., Birch, C.S., & Allan, K. (1998). Dissociation of the neural correlates of implicit and explicit memory. Nature, 392, 595– 598.

Rugg, M.D., Schloerscheidt, A.M., & Mark, R.E. (1998). An electrophysiological comparison of two indices of recollection. Journal of Memory & Language, 39, 47-69.

Smith, M.E. (1993). Neurophysiological manifestations of recollective experience during recognition memory judgments. Journal of Cognitive Neuroscience, 5, 113.

Spencer, K. M., Vila Abad, E., & Donchin, E. (2000). On the search for the neurophysiological manifestation of recollective experience. Psychophysiology, 37, 494-506.

Second, the parietal old/new effect is sensitive to variables thought to affect recollection more than familiarity such as depth of processing [40,41,57,61]. Third, when subjects are asked to introspectively differentiate words specifically ‘remembered’ from those merely ‘known’ to be old, larger parietal old/new effects are associated with ‘remembering’ than ‘knowing’ [14,59,63] (but also see Ref. [65]).

[14] E. Duzel, A.P Yonelinas, G.R. Mangun, H.-J. Heinze, E. Tulving, Event-related potential correlates of two states of conscious awareness in memory, Proc. Natl. Acad. Sci. USA 94 (1997) 5973-5978.

[40] K.A. Paller, M. Kutas, Brain potentials during memory retrieval provide neurophysiological support of the distinction between conscious recollection and priming, J. Cogn. Neurosci. 4 (1992) 375-391.

[41] K.A. Paller, M. Kutas, H.K. McIsaac, Monitoring conscious recollection via the electrical activity of the brain, Psychol. Sci. 6 (1995) 107-111.

[57] M.D. Rugg, K. Allan, C.S. Birch, Electrophysiological evidence for the modulation of retrieval orientation by depth of study processing, J. Cogn. Neurosci. 12 (2000) 664-678.

[59] M.D. Rugg, A.M. Schloerscheidt, R.E. Mark, An electrophysiological comparison of two indices of recollection, J. Mem. Lang. 39 (1998) 47-69.

[61] M.D. Rugg, P Walla, A.M. Schloerscheidt, P.C. Fletcher, C.D. Frith, R.J. Dolan, Neural correlates of depth of processing effects on recollection: evidence from brain potentials and positron emission tomography, Exp. Brain Res. 123 (1998) 18-23.

[63] M.E. Smith, Neurophysiological manifestations of recollective experience during recognition memory judgments, J. Cogn. Neurosci. 5 (1993) 1-13.

[65] K.M. Spencer, E. Vila Abad, E. Donchin, On the search for the neurophysiological manifestation of recollective experience, Psychophysiology 37 (2000) 494-506.

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[5.] Jm/Fragment 282 01 - Diskussion
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[In any] case, increased cortical activation is predicted by both the Standard Theory of Consolidation and Multiple Trace Theory, which both suggest that cortical-cortical connections will be strengthened as a memory is consolidated. However, Multiple Trace Theory emphasizes the importance of repeated retrieval for reconsolidation rather than the mere passage of time, while Standard Theory does not directly address this issue. We assume that these cortical patterns of activity are related to the behavioral changes described earlier, but further research is needed to clarify how the specific behavioral changes are related to neuroimaging changes. Increased cortical activation is predicted by both the standard theory of consolidation and MTT, which suggest that cortical-cortical connections will be strengthened as a memory is consolidated. However, MTT emphasizes the importance of repeated retrieval for reconsolidation rather than the mere passage of time, while standard theory does not directly address this issue. We assume that these cortical increases are related to the behavioral changes described earlier, but further research is needed to clarify how the specific behavioral changes are related to changes in fMRI signal.
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[6.] Jm/Fragment 058 06 - Diskussion
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The National Adult Reading Test (NART; Nelson, 1982; NART-2; Nelson & O’Connell, 1978; Nelson & Willison, 1991) has become among the most widely used retrospective estimators of premorbid level of intellectual functioning in neuropsychological practice and research concerning a wide range of conditions. Its use in estimating patients’ intellectual level prior to the onset of suspected dementia, for purposes of making comparisons with current levels of neuropsychological functioning, has become widespread.

Nelson, H.E. & O’Connell, A. (1978). Dementia : The estimation of pre-morbid intelligence levels using the new adult reading test. Cortex, 14, 234-244.

Nelson, H.E. & Willison, J. (1991). National Adult Reading Test (NART): Test manual. Second Eition. Windsor, UK: NFER Nelson. Neurology, 391(3), 293-321.

Nelson, H.E. (1982). National Adult Reading Test (NART): Test manual. Windsor, UK: NFER Nelson.

[Page 291]

The National Adult Reading Test (NART; Nelson, 1982, 1991) has become amongst the most widely used retrospective estimators of premorbid level of intellectual functioning in neuropsychological practice and research concerning a wide range of conditions. Its use in estimating patients’ intellectual level prior to the onset of suspected dementia, for purposes of making comparisons with current

[Page 292]

levels of neuropsychological functioning, has become widespread.


Nelson, H.E., 1982. National Adult Reading Test. NFER-Nelson, Windsor, UK.

Nelson, H.E., 1991. National Adult Reading Test, 2nd ed. NFER-Nelson, Windsor, UK.

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[7.] Jm/Fragment 281 01 - Diskussion
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[Evidence supporting this view comes from] neuroimaging studies showing that retrieval of detailed episodic memories activates the hippocampus irrespective of how old these memories are (e.g., Maguire et al., 2001; Rekkas & Constable, 2005) and from studies showing that remote episodic memories retrieved by amnesic patients lack the detail present in remote episodic memories of an individual with an intact hippocampus (Moscovitch et al., 2005).

Maguire, E.A., Vargha-Khadem, F., & Mishkin, M. (2001). The effects of bilateral hippocampal damage on fMRI regional activations and interactions during memory retrieval. Brain, 124, 1156–1170.

Moscovitch, M., Rosenbaum, R.S., Gilboa, A., Addis, D.R., Westmacott, R., & Grady, C. (2005). Functional neuroanatomy of remote episodic and semantic and spatial memory: a unified account based on multiple trace theory. Journal of Anatomy, 207, 35–66.

Rekkas, P.V. & Constable, T. (2005). Evidence that autobiographical memory retrieval does not become independent of the hippocampus: An fMRI study contrasting very recent with remote events. Journal of Cognitive Neuroscience, 17, 1950–1961.

Evidence supporting this view comes from neuroimaging studies showing that retrieval of detailed episodic memories activates the hippocampus no matter how old these memories are [14–18] and from studies showing that remote episodic memories retrieved by amnesic patients lack the detail present in remote episodic memories retrieved by an individual with an intact hippocampus [19].

[14] E. A. Maguire, R. N. A. Henson, C. J. Mummery, and C. D. Frith, “Activity in prefrontal cortex, not hippocampus, varies parametrically with the increasing remoteness of memories,” NeuroReport, vol. 12, no. 3, pp. 441–444, 2001.

[15] R. Lee, L. Nadel, and K. Keil, “Hippocampal complex and retrieval of recent and very remote autobiographical memories: evidence from functional magnetic resonance imaging in neurologically intact people,” Hippocampus, vol. 11, no. 6, pp. 707–714, 2001.

[16] A. Gilboa, G. Winocur, C. L. Grady, S. J. Hevenor, and M. Moscovitch, “Remembering our past: functional neuroanatomy of recollection of recent and very remote personal events,” Cerebral Cortex, vol. 14, no. 11, pp. 1214–1225, 2004.

[17] S. Steinvorth, B. Levine, and S. Corkin, “Medial temporal lobe structures are needed to re-experience remote autobiographical memories: evidence from H.M. and W.R.,” Neuropsychologia, vol. 43, no. 4, pp. 479–496, 2005.

[18] P. V. Rekkas and R. T. Constable, “Evidence that autobiographical memory retrieval does not become independent of the hippocampus: an fMRI study contrasting very recent with remote events,” Journal of Cognitive Neuroscience, vol. 17, no. 12, pp. 1950–1961, 2005.

[19] M. Moscovitch, R. S. Rosenbaum, A. Gilboa, et al., “Functional neuroanatomy of remote episodic, semantic and spatial memory: a unified account based on multiple trace theory,” Journal of Anatomy, vol. 207, no. 1, pp. 35–66, 2005.

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[8.] Jm/Fragment 280 18 - Diskussion
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The pattern of dipoles found herein conforms to a greater extent to the Multiple Trace Theory proposed by Nadel and Moscovitch (1997) which posits that the establishment of long-term memories involves a lengthy interaction between the hippocampal region of the medial temporal lobes (MTLs) and neocortical regions both adjacent to the MTL (e.g., perirhinal and parahippocampal cortices) and at a distance (e.g., prefrontal cortex). Unlike standard theory, Multiple Trace Theory posits that the hippocampus remains an integral part of the memory trace and is thus always involved in retrieval of long-term episodic memories regardless of the age of the memory. Nadel and Moscovitch [13] developed an alternative theory of memory consolidation, known as the multiple trace theory (MTT). Similar to the standard theory of consolidation, MTT posits that the establishment of long-term memories involves a lengthy interaction between the hippocampal region of the medial temporal lobes (MTLs) and neocortical regions both adjacent to the MTL (e.g., perirhinal and parahippocampal cortices) and at a distance (e.g., prefrontal cortex). [...] Unlike standard theory, MTT posits that the hippocampus remains an integral part of the memory trace and is thus always involved in retrieval of long-term episodic memories regardless of the age of the memory.
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[9.] Jm/Fragment 153 01 - Diskussion
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[This overriding experimental context diminishes the salience of any environmental] manipulations between study and test. Fernández and Glenberg’s proposal has received some empirical support from a study in which a radical context change was employed, with subjects’ recognition memory being tested over the telephone when they were at home (Canas & Nelson, 1986). This overriding experimental context diminishes the salience of any environmental manipulations between study and test. Fernandez and Glenberg's intriguing proposal has received some empirical support from a study in which a radical context change was employed, with subjects' recognition memory being tested over the telephone when they were at home (Canas & Nelson, 1986).
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[10.] Jm/Fragment 152 10 - Diskussion
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Indeed, Baddeley and colleagues (Baddeley & Woodhead, 1982; Godden & Baddeley, 1980) have proposed that recognition, unlike recall, is not contextually dependent unless context and stimulus are interactively encoded or integrated at study. Thus, the contextual encoding of the environmental features that took place did so in the absence of demands for intentional interactive processing.

[...] The need for a within-subjects design with respect to global context manipulations is evident when one considers the potential for significant criterion changes for study items tested in different environmental conditions. A within-subjects design would avoid this problem in the global context manipulation. [...] Furthermore, regarding the Experimental Context hypothesis, Fernández and Glenberg (1985) proposed that laboratory context manipulations are inherently ineffective because, from the subject’s perspective, all environmental context changes occur within the broader “Experimental context.”

[page 225]

The need for a within-subjects design with respect to global context manipulations is evident when one considers the potential for significant criterion changes for study items tested in different environmental conditions. A within-subjects design avoids this problem in the global context manipulation.

[page 231]

To account for this dissociation between memory measures, Baddeley and his colleagues (Baddeley& Woodhead, 1982; Godden & Baddeley, 1980) have proposed that recognition, unlike recall, is not contextually dependent unless context and stimulus are interactively encoded or integrated at study. [...] The contextual encoding of the environmental features that took place did so in the absence of demands for intentional interactive processing.

[page 232]

The experimental context hypothesis. Fernandez and Glenberg (1985) [made one of the more rigorous and systematic attempts to demonstrate context effects on memory. After failing to find context-dependent recognition or recall in over 300 subjects, they] proposed that laboratory context manipulations are inherently ineffective because, from the subject's perspective, all environmental context changes occur within the broader "experimental context."

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[11.] Jm/Fragment 151 01 - Diskussion
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[The representation can be] considered in a state of “decontextualization,” whereby it can be activated and the corresponding item can be recognized without the reinstatement of cues present at encoding.

In a number of studies of face recognition, somewhat similar to abstract stimulus recognition, changes in local contexts such as semantic labels, face associates, or background cues have resulted in decreased recognition accuracy. In addition, in several demonstrations, changes in global context have resulted in decreased recognition for unfamiliar faces (e.g., Cann & Ross, 1989; Gage & Safer, 1985; Malpass & Devine, 1981). Abstract stimulus recognition, like face recognition, may rely on context reinstatement to a greater extent than word recognition does because of the importance of stimulus novelty. With verbal stimuli, the identification of a letter string as a word requires experience with that particular letter string; hence it can hardly be considered a novel stimulus.

[page 224]

The representation can be considered in a state of "decontextualization," whereby it can be activated and the corresponding item can be rec-

[page 225]

ognized without the reinstatement of cues present at encoding.2

[...]

[...] In a number of studies of face recognition, changes in local contexts such as semantic labels, face associates, or background cues have resulted in decreased recognition accuracy. In addition, in several demonstrations, changes in global context have resulted in decreased recognition for unfamiliar faces (see, e.g., Cann & Ross, 1989; Gage & Safer, 1985; Malpass & Devine, 1981).

Face recognition may rely on context reinstatement more than word recognition does because of the importance of stimulus novelty. With verbal stimuli, the identification of a letter string as a word requires experience with that particular letter string; hence it can hardly be considered a novel stimulus.


2. [...]

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The source is mentioned on the previous page as well as on the next page. But neither mention suggests that any text has been quoted from the source.

The parallel text begins on the previous page: Jm/Fragment_150_06

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[12.] Jm/Fragment 150 06 - Diskussion
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Empirical support for the notion that stimulus familiarity plays a role takes several forms. Davies and Milne (1982) showed participants pictures of both novel and famous faces while varying background, pose, and expression. They found reduced recognition performance for novel, but not famous, faces as a function of all three changes, thereby demonstrating differential local context effects for familiar as opposed to novel faces. As such, it would seem plausible that modulation by the environmental context might differ for novel and familiar stimuli. In any case, the important role of stimulus familiarity is also supported by findings within the domain of animal learning, whereby context effects on recognition-like tasks have traditionally been more reliable. Recognizing the importance of the relation between stimulus and context, Lubow, Rifkin, and Alek (1976) showed that exposing a stimulus prior to presenting it in a novel environmental context (i.e., making it familiar) enhanced perceptual learning, in comparison with the simple presentation of a novel stimulus in the learning context.

There are other salient reasons why a stimulus attribute such as familiarity might be a parameter of contextual modulation. Whether contextual attributes such as temporal or spatial information are present or absent constitutes one of the critical distinctions that Tulving (1972) makes between episodic and semantic memory systems. According to Tulving, multiple presentations of an item allow that item to be abstracted from its context. As the item representation becomes progressively more semantic in nature, its reliance on specific contextual attributes for recognition is diminished.


Davis [sic], G. & Milne, A. (1982). Recognising faces in and out of context. Current Psychological Research, 2, 235-246.

Lubow, R. E., Rifkin, B., & Alek, M. (1976). The context effect: the relationship between stimulus pre-exposure and environmental pre-exposure determines subsequent learning. Journal of Experimental Psychology: Animal Behavior Processes, 2, 38-47.

Tulving, E. (1972). Episodic and semantic memory. In E. Tulving & W. Donaldson (Eds.), Organization of Memory (pp. 382-404). New York: Academic Press.

Empirical support for the notion that stimulus familiarity plays a role takes several forms. Davies and Milne (1982) showed subjects pictures of both novel and celebrity faces while varying background, pose, and expression. They found reduced recognition performance for novel, but not celebrity, faces as a function of all three changes. Unfortunately, they used a small number of faces and the performance for the familiar faces was at ceiling, causing some interpretive problems with their data. Yet the demonstration of differential local context effects for familiar as opposed to novel faces was encouraging. It seemed plausible that modulation by the environmental context might differ for novel and familiar stimuli as well.

The important role of stimulus familiarity is also supported by results in the domain of animal learning, where context effects on recognition-like tasks have traditionally been more reliable. Recognizing the importance of the relation between stimulus and context, Lubow, Rifkin, and Alek (1976) showed that exposing a stimulus prior to presenting it in a novel environmental context (i.e., making it familiar) enhanced perceptual learning, in comparison with the simple presentation of a novel stimulus in the learning context.

There are other salient reasons why a stimulus attribute like familiarity might be a parameter of contextual modulation. Whether contextual attributes such as temporal or spatial information are present or absent constitutes one of the critical distinctions that Tulving (1972) makes between episodic and semantic memory systems. According to Tulving, multiple presentations of an item allow that item to be abstracted from its context. As the item representation becomes progressively more semantic in nature, its reliance on specific contextual attributes for recognition is diminished.


DAVIES, G., & MILNE, A. (1982). Recognising faces in and out of context. Current Psychological Research, 2, 235-246.

LUBOW, R. E., RIFKIN, B., & ALEK, M. (1976). The context effect: The relationship between stimulus pre-exposure and environmental pre-exposure determines subsequent learning. Journal of Experimental Psychology: Animal Behavior Processes, 2, 38-47.

TULVING, E. (1972). Episodic and semantic memory. In E. Tulving & W. Donaldson (Eds.), Organization of memory (pp. 382-404). New York: Academic Press.

Anmerkungen

The source is mentioned further up, but without indication that the following two paragraphs might have been taken from it. Continued on the next page: Jm/Fragment_151_01

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[13.] Jm/Fragment 009 01 - Diskussion
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These axons constitute the loop’s first connection, together with the granular cells of the dentate gyrus (Anderson et al., 2007; Amaral & Witter, 1989; see Figure 1.1). From these cells, mossy fibres in turn project to make the loop’s second connection, with the dendrites of the pyramidal cells in area CA3. The axons of these cells divide into two branches. One branch forms the commissural fibres that project to the controlateral hippocampus via the corpus callosum. The other branch forms the Schaffer collateral pathways that make the third connection in the loop, with the pyramidal cells of area CA1 (Ishizuka, Weber & Amaral, 1990). The axons of the cells in CA1 then project to the neurons of the subiculum and of the EC. The receiving portion of the HF thus consists of the dentate gyrus, whereas the sending portion consists of the subiculum (see Figure 1.4). The axons of the large pyramidal neurons of the subiculum then project to the subcortical nuclei via the fimbria, a thin tract of white matter located at the inner edge of the hippocampus. Finally, the information returns to the sensory cortical areas from which it came prior to hippocampal processing. These axons make the loop’s first connection, with the granule cells of the dentate gyrus.

From these cells, the mossy fibres in turn project to make the loopÂ’s second connection, with the dendrites of the pyramidal cells in area CA3.

The axons of these cells divide into two branches. One branch forms the commissural fibres that project to the controlateral hippocampus via the corpus callosum. The other branch forms the Schaffer collateral pathways that make the third connection in the loop, with the cells in area CA1.

[...]

Lastly, the axons of the cells in CA1 project to the neurons of the subiculum and of the entorhinal cortex. The receiving portion of the hippocampal formation thus consists of the dentate gyrus, while the sending portion consists of the subiculum. The axons of the large pyramidal neurons of the subiculum then project to the subcortical nuclei via the fimbria, a thin tract of white matter at the inner edge of the hippocampus. Lastly, the information returns to the sensory cortical areas from which it came before it was processed by the hippocampus.

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[14.] Jm/Fragment 045 01 - Diskussion
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[However, Tronel and colleagues (2005), in a study adopting inhibitory avoidance learning in rats, did not find evidence that] reconsolidation is functionally involved in linking new information to a reactivated memory. Using the doubly dissociable mechanisms of inhibitory avoidance memory consolidation and reconsolidation, these researchers demonstrated that second-order conditioning recruited consolidation processes in a selective manner. However, according to Tronson and Taylor (2007), linking new information to an old memory can be conceptualized as new learning based upon evoked memories, which would be expected to necessitate consolidation mechanisms rather than true memory updating. Lee (2008) recently directly addressed the functional role of memory reconsolidation employing the doubly dissociable mechanisms of consolidation and reconsolidation in hippocampal contextual fear memories, finding that a basic form of memory updating, namely strengthening through a further learning episode, was selectively dependent upon reconsolidation mechanisms. Thus, as suggested by Lee(2009), memory reconsolidation might prove to be the mechanism by which memories are updated through further experience, although it remains to be determined whether reconsolidation has a similar functional role in other forms of memory updating, such as memory weakening or changes in memory content.

Although the mechanisms of memory reconsolidation largely recapitulate those of initial consolidation, there are notable dissociations between the two (see Moore & Roche, 2007 and Alberini, 2005 for a comprehensive review). In particular, there is evidence that reconsolidation recruits specific mechanisms that are not crucially involved in consolidation. The reconsolidation, but not consolidation, of discrete fear memories is vulnerable to ßadrenoceptor blockade (Debiec & LeDoux, 2004). Moreover, the cellular mechanisms of memory consolidation and reconsolidation for both contextual fear (Lee et al., 2004) and inhibitory avoidance (Taubenfeld et al., 2001; Milekic et al., 2007) are doubly dissociable. As such, reconsolidation is a neurobiologically distinct memory process, which is [increasingly associated with specific cellular mechanisms, such as the expression of the immediate-early gene zif268 (Lee et al., 2004, 2005).]

[page 2]

Moreover, a prior study of inhibitory avoidance learning in rats did not provide evidence that reconsolidation is functionally involved in linking new information to a reactivated memory [19]. Using the doubly dissociable mechanisms of inhibitory avoidance memory consolidation and reconsolidation, Tronel et al. showed that second-order conditioning recruited consolidation processes selectively [19]. However, linking new information to an old memory can be viewed simply as new learning based upon evoked memories, which would be expected to necessitate consolidation mechanisms, rather than true memory updating [5]. In a study designed to address directly the functional role of memory reconsolidation, I similarly capitalised on the doubly dissociable mechanisms of consolidation and reconsolidation in hippocampal contextual fear memories. A simple form of memory updating, namely strengthening through a further learning episode, was dependent selectively upon reconsolidation mechanisms [20]. Therefore, memory reconsolidation may well prove to be the mechanism by which memories are updated through further experience, though it remains to be determined whether reconsolidation plays a similar functional role in other forms of memory updating, such as memory weakening or changes in memory content.

[page 3]

Indeed, although the mechanisms of memory reconsolidation largely recapitulate those of initial consolidation, there are notable dissociations between the two (See Alberini, 2005 [6] for a comprehensive review). In particular, there is evidence that reconsolidation recruits specific mechanisms that are not critically involved in consolidation. The reconsolidation, but not consolidation, of discrete fear memories is vulnerable to β-adrenergic receptor blockade [21]. Moreover, the cellular mechanisms of memory consolidation and reconsolidation for both contextual fear [22] and inhibitory avoidance [23, 24] are doubly dissociable. [Such double dissociations rule out simple quantitative or non-specific factors, such as time or the absence of the highly motivating footshock reinforcer, as being the cause of differences between the mechamisms of consolidation and reconsolidation.] Therefore, reconsolidation is a neurobiologically-distinct memory process, which is beginning to be associated with specific cellular mechanisms, such as the expression of the immediate-early gene zif268 [22, 25].


5. Tronson NC, Taylor JR. Molecular mechanisms of memory reconsolidation. Nat Rev Neurosci. 2007; 8:262–275. [PubMed: 17342174]

6. Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends Neurosci. 2005; 28:51–56. [PubMed: 15626497]

19. Tronel S, et al. Linking new information to a reactivated memory requires consolidation and not reconsolidation mechanisms. PLoS Biol. 2005; 3:e293. [PubMed: 16104829]

20. Lee JLC. Memory reconsolidation mediates the strengthening of memories by additional learning. Nat Neurosci. 2008; 11:1264–1266. [PubMed: 18849987]

21. Debiec J, LeDoux JE. Disruption of reconsolidation but not consolidation of auditory fear conditioning by noradrenergic blockade in the amygdala. Neuroscience. 2004; 129:267–272. [PubMed: 15501585]

22. Lee JLC, et al. Independent cellular processes for hippocampal memory consolidation and reconsolidation. Science. 2004; 304:839–843. [PubMed: 15073322]

23. Taubenfeld SM, et al. The consolidation of new but not reactivated memory requires hippocampal C/EBP beta. Nat Neurosci. 2001; 4:813–818. [PubMed: 11477427]

24. Milekic MH, et al. Temporal requirement of C/EBPbeta in the amygdala following reactivation but not acquisition of inhibitory avoidance. Learn Mem. 2007; 14:504–511. [PubMed: 17644752]

25. Lee JLC, et al. Disrupting reconsolidation of drug memories reduces cocaine seeking behavior. Neuron. 2005; 47:795–801. [PubMed: 16157275]

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[15.] Jm/Fragment 029 04 - Diskussion
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Human and animal studies firmly establish that the high levels of glucocorticoids released during stress impair the function of the hippocampus, thereby weakening or completely disrupting those aspects of contextual and episodic memory subserved by this structure (De Quervain et al., 2000, Diamond & Rose, 1994, Lupien et al., 1998; Nadel & Jacobs, 1998; Newcomer et al., 1999). We reason herein that if stress interferes with the normal functions of the hippocampus, and the hippocampus is central to context effects in memory, then stress might interfere with those forms of memory dependent upon context and the binding it supports. Thus, we presently postulate that manipulations adversely affecting contextual encoding and retrieval, such as stress, should interfere with memory retrieval, [...] We argue that manipulations adversely affecting contextual encoding and retrieval should interfere with veridical remembering. Stress could be one such factor. [...] Human and animal studies firmly establish that the high levels of glucocorticoids released during stress impair the function of the hippocampus, weakening or completely disrupting those aspects of contextual and episodic memory subserved by this structure (De Quervain et al. 2000,Diamond and Rose 1994, Lupien et al. 1998, Nadel and Jacobs 1998, Newcomer et al. 1999).

We reasoned that if stress interferes with the normal functions of the hippocampus, and the hippocampus is central to context effects in memory, then stress might interfere with those forms of memory depending on context and the binding it supports.

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[16.] Jm/Fragment 016 23 - Diskussion
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Thus, memories can lose their “context” dependence, becoming less “episodic” and more “semantic” in nature. As such, the “context” representation that supports [conditioned fear after several weeks is a representation based on elements present in the test situation rather than a configural representation of the whole.] More specifically, memories can lose their “context” dependence, becoming less “episodic” and more “semantic” in nature. [...]

[...]

[Instead of assuming that “memory” is either transferred from hippocampus to neocortex, or given independent status within neocortex after a period of requiring hippocampal help in retrieval,] one can best account for the data by assuming that the “context” representation that supports conditioned fear after several weeks is a representation based on elements in the test situation rather than a configural representation of the whole.

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The copied text is continued on the next page: Jm/Fragment_017_01

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(Hindemith) Schumann

[17.] Jm/Fragment 015 01 - Diskussion
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Several authors have suggested that hippocampal memory functions are mediated by circuitry involving the entorhinal cortex, anterior thalamus, prefrontal cortex, and retrosplenial cortex (Aggleton & Brown, 1999; Eichenbaum, 2000; Suzuki & Eichenbaum, 2000; Smith et al., 2004; Wiltgen et al., 2004; Siapas et al., 2005). Several authors have suggested that hippocampal memory functions are mediated by circuitry involving the entorhinal cortex, anterior thalamus, prefrontal cortex, and retrosplenial cortex (Aggleton and Brown, 1999; Eichenbaum, 2000; Suzuki and Eichenbaum, 2000; Smith et al., 2004; Wiltgen et al., 2004; Siapas et al., 2005).
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[18.] Jm/Fragment 014 04 - Diskussion
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Indeed, an extensive literature involving brain lesions has implicated the hippocampus in context processing (for review, see Myers & Gluck, 1994; Anagnostaras et al., 2001; Maren, 2001). For example, hippocampal lesions impair conditioned fear responses to contextual stimuli (Kim & Fanselow, 1992; Phillips & LeDoux, 1992), and lesions of the hippocampus or entorhinal cortex render subjects insensitive to changes in the context (Penick & Solomon, 1991). Also, subjects with fornix lesions have been shown to be severely impaired in learning two different discrimination tasks that were trained in different contexts (Smith et al., 2004). In the same subjects, context-specific neuronal firing patterns were degraded in structures receiving hippocampal input via the fornix (i.e., anterior thalamus and cingulate cortex). Such findings infer that the hippocampus generates a unique context code that modulates processing in downstream structures.

Furthermore, the hippocampus has been widely implicated in episodic memory (e.g., Tulving & Markowitsch, 1998; Aggleton & Brown, 1999; Eichenbaum & Cohen, 2001). Hippocampal neurons respond preferentially to conjunctions of stimuli, such as the concurrence [sic] of a conditional stimulus and a place (Wood et al., 1999; Moita et al., 2003), and spatial firing can be contingent on past or future actions (Frank et al., 2000; Wood et al., 2000; Ferbinteanu & Shapiro, 2003). Findings such as these suggest that hippocampal neurons encode the relations among stimuli in the interest of episodic memory. Smith and Mizumori (2006) recently suggested that the hippocampus contributes contextual information to a wider circuitry for the formation of episodic memories. Therefore, episodic memory may be mediated by extended circuitry that includes, but is not limited to, the hippocampus.

[page 3154]

An extensive literature involving brain lesions has implicated the hippocampus in context processing (for review, see Myers and Gluck, 1994; Anagnostaras et al., 2001; Maren, 2001). For example, hippocampal lesions impair conditioned fear responses to contextual stimuli (Kim and Fanselow, 1992; Phillips and LeDoux, 1992), and lesions of the hippocampus or entorhinal cortex render subjects insensitive to changes in the context (Penick and Solomon, 1991; Freeman et al., 1997). Also, subjects with fornix lesions were severely impaired in learning two different discrimination tasks that were trained in different contexts (Smith et al., 2004). In the same subjects, context-specific neuronal firing patterns were degraded in structures receiving hippocampal input via the fornix (anterior thalamus and cingulate cortex). These findings suggested that the hippocampus generates a unique context code that modulates processing in downstream structures.

[page 3161]

The hippocampus has been widely implicated in episodic memory (Tulving and Markowitsch, 1998; Aggleton and Brown, 1999; Eichenbaum and Cohen, 2001). Hippocampal neurons respond preferentially to conjunctions of stimuli, such as the co-occurrence of a conditional stimulus and a place (Wood et al., 1999; Moita et al., 2003), and spatial firing can be contingent on past or future actions (Frank et al., 2000; Wood et al., 2000; Ferbinteanu and Shapiro, 2003). Findings such as these suggest that hippocampal neurons encode the relations among stimuli in the interest of episodic memory. [...]

[...]

[...] Therefore, episodic memory may be mediated by extended circuitry that includes, but is not limited to, the hippocampus. [...] The present results suggest that the hippocampus contributes contextual information to a wider circuitry for the formation of episodic memories.

Anmerkungen

Smith and Mizumori (2006) are given as reference for one result. However, this refers not to the source of the copied text, but to a different publication (see list of references):

Smith, D.M. & Mizumori, S.J.Y. (2006). Hippocampal place cells, context, and episodic memory. Hippocampus, 16, 716-729.

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[19.] Jm/Fragment 012 01 - Diskussion
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[The perirhinal cortex receives inputs including from visual areas in the] ventral temporal cortex and the ventral and dorsal banks of the superior temporal sulcus (Lavenex & Amaral, 2000; Suzuki & Amaral, 1994a,b).

[Figure 1.4]

The neocortical connections of parahippocampal and perirhinal cortices are complementary (Burwell & Amaral, 1998; Suzuki & Amaral, 1994a; see Figure 1.4). Both the parahippocampal and perirhinal cortices feed information into the entorhinal cortex. The parahippocampal cortex mainly projects to the medial entorhinal area, whereas the perirhinal mainly projects to the lateral entorhinal area. The entorhinal cortex, in turn, projects to the HF. These parallel pathways, however, are interconnected with a substantial projection from parahippocampal cortex to perirhinal cortex, in addition to connections between the lateral and medial areas of the entorhinal cortex. Thus the anatomy of the cortico parahippocampal-hippocampal system is best described as including both parallel and hierarchical components, positioning it well to integrate diverse informational sources important to memory (Burwell, 2000; Furtak et al., 2007; Lavenex & Amaral 2000; Witter et al., 2000).

The neocortical connections of parahippocampal and perirhinal cortices are complementary (Burwell and Amaral 1998; Suzuki and Amaral 1994a). Both the parahippocampal and perirhinal cortices feed information into the entorhinal cortex. The parahippocampal cortex projects largely to the medial entorhinal area, whereas the perirhinal projects largely to the lateral entorhinal area. The entorhinal cortex, in turn, projects to the hippocampal formation. These parallel pathways, however, are interconnected with a substantial projection from parahippocampal cortex to perirhinal cortex, in addition to connections between the lateral and medial areas of the entorhinal cortex. Thus the anatomy of the cortico-parahippocampal-hippocampal system is best described as including both parallel and hierarchical components, positioning it well to integrate diverse informational sources important to memory (Burwell 2000; Furtak et al. 2007; Lavenex and Amaral 2000; Witter et al. 2000).

[...] The perirhinal cortex receives inputs including from visual areas in the ventral temporal cortex and the ventral and dorsal banks of the superior temporal sulcus (Lavenex and Amaral 2000; Suzuki and Amaral 1994a,b).

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[20.] Jm/Fragment 011 01 - Diskussion
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The importance of the MTL as a memory system is attributable to its connectivity with the broader neocortex. Multiple uni- and polymodal cortical regions project to the parahippocampal and perirhinal cortices (Burwell & Amaral, 1998; Schmahmann & Pandya, 2006; Suzuki & Amaral, 1994a). These cortical projections encompass two parallel pathways. The parahippocampal cortex receives inputs from visual association areas, retrosplenial cortex, the dorsal bank of the superior temporal sulcus, and the parietal lobe, among other regions. The centrality of the MTL memory system extends to its connectivity with the broader neocortex. Multiple uni- and polymodal cortical regions project to the parahippocampal and perirhinal cortices (Burwell and Amaral 1998; Schmahmann and Pandya 2006; Suzuki and Amaral 1994a). The cortical projections encompass two parallel pathways. The parahippocampal cortex receives inputs from visual association areas, retrosplenial cortex, the dorsal bank of the superior temporal sulcus, and the parietal lobe, among other regions.
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[21.] Jm/Fragment 010 07 - Diskussion
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On a larger scale, the medial temporal lobe (MTL) encompasses anatomically related structures including the the [sic] hippocampal formation and adjacent parahippocampal, perirhinal, and entorhinal cortices, which lie along the parahippocampal gyrus (collectively referred to as the parahippocampal region; see Witter et al., 2000). The complex anatomy of the MTL has led to a debate about the nature of the contributions of subregions of the MTL and whether they are associated with functionally distinct processes or act collectively as an integrated system (e.g., Eichenbaum et al., 2007; Squire et al., 2004). The MTL encompasses anatomically related structures including the hippocampal formation and adjacent parahippocampal, perirhinal, and entorhinal cortices, which lie along the parahippocampal gyrus (collectively referred to as the parahippocampal region) (see Witter et al. 2000). The complex anatomy of the MTL has led to a debate about the nature of the contributions of subregions of the MTL and whether they are associated with functionally distinct processes or act collectively as an integrated system (e.g., Eichenbaum et al. 2007; Squire et al. 2004).
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[For example,] Walker and colleagues (2003) demonstrated reconsolidation in humans using a procedural motor-skill task that involved finger-tapping a simple sequence (e.g., 4-1-3-2). Twenty-four hours after original exposure to the sequence, participants briefly rehearsed the sequence, thereby reactivating it, and learned a second sequence (e.g., 2-3-1-4). When tested on Day 3, accuracy performance for Sequence 1 was significantly impaired relative to control subjects who did not rehearse Sequence 1 before learning Sequence 2. This shows that the reactivation of the memory for Sequence 1 on Day 2 destabilized it such that a competing motor pattern could interfere with the memory trace. Further, Galluccio (2005) and Galluccio and Rovee-Collier (2005), adopting a conditioning-based paradigm, investigated the fate of reactivated memories in infants trained to kick their foot to activate a mobile. After a delay period, infants were reminded of the event: The moving mobile was presented for a brief period during which it was no longer attached to the baby’s foot. Following reactivation, one group of infants learned to move a novel mobile. One day later, infants who were exposed to the novel mobile showed a modification of the reactivated memory such that they no longer recognized the original mobile reacted only to the novel one. Walker et al. (2003) recently demonstrated reconsolidation effects in humans. Participants were trained on a procedural motor-skill task that involved finger-tapping a simple sequence (e.g., 4-1-3-2). Twenty-four hours later they briefly rehearsed the sequence (reactivating it) and learned a second sequence (e.g., 2-3- 1-4). When tested on Day 3, accuracy performance for Sequence 1 was significantly impaired in comparison to a group of participants who did not rehearse Sequence 1 before learning Sequence 2. This shows that the reactivation of the memory for Sequence 1 on Day 2 destabilized it such that a competing motor pattern could interfere.

Galluccio (2005) and Galluccio and Rovee-Collier (2005) investigated the fate of reactivated memories in infants trained to kick their foot to activate a mobile. After a delay, infants were reminded of the event: The moving mobile was presented for a brief period during which it was no longer attached to the baby’s foot. After reactivation, one group of infants learned to move a novel mobile. One day later, infants who were exposed to the novel mobile showed a modification of the reactivated memory in that they no longer recognized the original mobile and solely reacted to the novel one.

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Further, the importance of stress and stress hormones during the different stages of memory processing, including reconsolidation, has been implicated in the literature (Diamond et al., 1996; Loscertales et al., 1998; Newcomer et al., 1994, 1999; Roozendaal, 2002). Stress and glucocorticoids (GCs) both enhance (Loscertales et al., 1998; Roozendaal, 2002) as well as impair (Diamond et al., 1996; Newcomer et al., 1994, 1999) memory consolidation, and memory retrieval is typically impaired (de Quervain et al., 1998; Kuhlmann et al., 2005). To date, only a few groups have studied the effects of stress or GCs on the reconsolidation of memory. Maroun and Akirav (2008) provided the first evidence that stress may exert an inhibitory effect on the reconsolidation of memory. They found that, in habituated (low arousal level) and nonhabituated (high arousal level) rats, exposure to an out-of-context stressor impaired long-term reconsolidation of object recognition memory. In a recent study conducted by Wang and colleagues (2008), morphine CPP was blocked in rats that received a cold-water stressor or corticosterone following a single-trial reactivation by disrupting reconsolidation of morphine reward memory. It was found that stress administered after drug-related memory retrieval significantly decreased subsequent recall through an impaired drug-related memory reconsolidation process, a result consistent with previous studies suggesting that stress impairs the reconsolidation of recognition memory (Maroun & Akirav 2008). However, little is known regarding the effects of stress on the reconsolidation of drug-related memories in humans. The importance of stress and stress hormone in the different stages of memory processes including reconsolidation has been implicated in the literature (Diamond et al. 1996; Loscertales et al. 1998; Newcomer et al. 1994, 1999; Roozendaal 2002). Stress and glucocorticoids enhance (Loscertales et al. 1998; Roozendaal 2002) as well as impair (Diamond et al. 1996; Newcomer et al. 1994, 1999) memory consolidation, and memory retrieval is usually impaired (de Quervain et al. 1998; Kuhlmann et al. 2005b). Moreover, in our recent study, we found that treatment with stress or corticosterone after a single memory reactivation blocks reconsolidation of a drug-related memory in rats. However, little is known regarding the effects of stress on reconsolidation of drug-related memories in human.

[page 6]

Only a few groups have studied the effects of stress or glucocorticoids on reconsolidation of memory. Maroun and Akirav (2008) provided the first evidence that stress might have an inhibitory effect on the reconsolidation of memory. They found that, in habituated (low arousal level) and nonhabituated (high arousal level) rats, exposure to an out-of-context stressor impaired long-term reconsolidation of objective recognition memory (Maroun and Akirav 2008). In our recent study, morphine CPP was blocked in rats that received a cold-water stress or corticosterone after a single-trial reactivation by disrupting reconsolidation of morphine reward memory (Wang et al. 2008). In this study, we found that stress after drug-related memory retrieval significantly decreased its subsequent recall through impaired drug-related memory reconsolidation process, a result consistent with the previous studies that stress impairs reconsolidation of recognition memory (Maroun and Akirav 2008; Wang et al. 2008).

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Using drug cues as reinforcers, investigators reported that the β-adrenoreceptor antagonist propranolol, administered after reactivation of cocaine or morphine conditioned place preference (CPP), impairs drug seeking via disruption of reconsolidation (Bernardi et al., 2006; Robinson & Franklin, 2007). Using drugs as reinforcers, investigators reported that the β-adrenoreceptor antagonist propranolol, administered after reactivation of cocaine or morphine conditioned place preference (CPP), impairs drug seeking via disruption of reconsolidation (Bernardi et al., 2006; Robinson and Franklin, 2007).
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[Alternately, a hypothesis based upon memory updating incorporates] both the principles of the dual state hypothesis (in that a requirement for updating depends upon the same conditions as those proposed to engage an encoding state), and can potentially account for other boundary conditions.

Further, Ortiz and Bermudez-Rattoni (2007) postulate reconsolidation as an ‘updating consolidation’ mechanism. Further to demonstrating that fully learned memories are not subject to reactivation-dependent amnesia, these researchers found in both spatial and taste memories that when learning had reached near-asymptotic levels, only partial amnesia resulted from reactivation and protein synthesis inhibition (Rodriguez-Ortiz et al., 2005, 2008). This partial amnesia was considered to reflect only the partial destabilization of the existing memory trace to enable updating. As such, this idea is not dissimilar to Alberini’s previously discussed contention that old memories can be updated, but not disrupted (2005). Moreover, Rodriguez- Ortiz and Bermudez-Rattoni suggest that reconsolidation associated response decrements do not reflect memory loss for the original consolidated memory but, rather, emanate from a failure to integrate new learning, thereby leading to interference. However, such an interpretation cannot account for recent findings in terms of contextual fear memories (e.g., Lee, 2008). If reconsolidation impairments result from new learning interfering with the stable old memory trace, disruption of the new learning itself should result in an unchanged memory (Lee, 2009). However, in Lee’s (2008) recent study, this is not what was observed when the consolidation-specific protein BDNF was knocked down2 in the hippocampus during memory strengthening/updating. Instead, while knocking down BDNF had no impact on memory strengthening, the modification of the old memory was completely dependent upon the reconsolidation-selective upregulation of zif268.


[2 Gene knockdown refers to techniques by which the expression of one or more of an organism's genes is reduced, either through genetic modification (a change in the DNA of one of the organism's chromosomes) or by treatment with a reagent such as a short DNA or RNA oligonucleotide with a sequence complementary to either an mRNA transcript or a gene.]

A hypothesis based upon memory updating, in contrast, both incorporates the principles of the dual state proposal (in that a requirement for updating depends upon the same conditions as those proposed to engage an encoding state), and can potentially account for other boundary conditions.

Boundary conditions on memory reconsolidation also influence a further hypothesis of memory updating that is superficially similar to that advanced here. Rodriguez-Ortiz & Bermudez-Rattoni [60] conceive of reconsolidation as an “updating consolidation” mechanism (Fig. 1B). As well as showing that fully-learned memories are not subject to reactivation-dependent amnesia, these authors observed in both spatial and taste memories that when learning had reached near-asymptotic levels, only partial amnesia resulted from reactivation and protein synthesis inhibition [43, 44]. This partial amnesia is inferred to reflect only the partial destabilisation of the existing memory trace to enable updating. As such, this idea is not dissimilar to Alberini’s suggestion that old memories can be updated, but not disrupted [6]. Moreover, Rodriguez-Ortiz & Bermudez-Rattoni suggest that reconsolidation-associated response decrements do not reflect memory loss for the original consolidated memory, but rather result from a failure to integrate new learning, leading to interference. However, such an interpretation cannot account for my recent results in contextual fear memories [20]. If reconsolidation impairments result from new learning interfering with the stable old memory trace, disruption of the new learning itself should result in an unchanged memory. This is not what was observed when the consolidation-specific protein BDNF was knocked down in the hippocampus during memory strengthening/updating. Instead, while knocking down BDNF had no impact on memory strengthening, the modification of the old memory was completely dependent upon the reconsolidation-selective upregulation of zif268.


6. Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends Neurosci. 2005; 28:51–56. [PubMed: 15626497]

20. Lee JLC. Memory reconsolidation mediates the strengthening of memories by additional learning. Nat Neurosci. 2008; 11:1264–1266. [PubMed: 18849987]

43. Rodriguez-Ortiz CJ, et al. Protein synthesis underlies post-retrieval memory consolidation to a restricted degree only when updated information is obtained. Learn Mem. 2005; 12:533–537. [PubMed: 16166395]

44. Rodriguez-Ortiz CJ, et al. Intrahippocampal anisomycin infusions disrupt previously consolidated spatial memory only when memory is updated. Neurobiol Learn Mem. 2008; 89:352–359. [PubMed: 18054256]

60. Rodriguez-Ortiz, CJ.; Bermudez-Rattoni, F. Memory reconsolidation or updating consolidation?. In: Bermudez-Rattoni, F., editor. Neural plasticity and memory: From genes to brain imaging. Taylor and Francis Group; 2007. p. 209-224.

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[Specifically, Alberini (2005) suggests that] repeated reactivations (which might be implicit during sleep) gradually increase memory stability as part of a lengthy consolidation process, such that when sufficient time has elapsed a memory can no longer be disrupted, but it can be added to or modified. Dudai and Eisenberg (2004) similarly integrate reconsolidation within a ‘lingering consolidation’ process, whereby the reactivation and reconsolidation cycle progressively stabilizes a memory. In contrast to such emphases on reconsolidation enhancing memory stability, memory updating does not require that reconsolidation has an endogenous role to play in the ongoing processing of a memory trace that requires no further modification. Indeed, the reverse has been suggested (see Lee, 2009), in that a memory will persist in a stable and fixed form only if reconsolidation is not engaged, given that reconsolidation is the mechanistic instantiation of memory updating. Thus, reconsolidation only plays a role in enhancing memory stability if such enhancement is dependent upon modification of the memory. Instead of focusing on reconsolidation constraints, Morris and colleagues (2006) argue instead for a mode-based explanation of reconsolidation according to which the dual activation of retrieval and encoding states drives reconsolidation processes. This model is well suited to account for situations wherein new experiences result in profound changes to the memory; a change in the location of an escape platform in a water maze being the example used for the delayed non-mapping to place task. However, it is not clear either how it might be adapted to conditions of more negligible memory modifications (e.g., strength), or whether the activation of an ‘encoding mode’ is sufficient to trigger reconsolidation. For example, extinction training involves both memory retrieval as well as new memory encoding, but under such circumstances reconsolidation is not obviously engaged (e.g., Lee et al., 2006; Suzuki et al., 2004; Pedreira & Moldonado, 2003). Moreover, the mode requirement appears to be an additional, as opposed to an alternative, boundary condition to those already discussed. Specifically, Alberini [6] suggests that repeated reactivations (which may be implicit during sleep) gradually increase memory stability as part of a lengthy consolidation process, such that when sufficient time has elapsed, a memory can no longer be disrupted, but can be added to or modified. Dudai & Eisenberg [8] similarly integrate reconsolidation within a “lingering consolidation” process, whereby the reactivation and reconsolidation cycle progressively stabilises a memory (Fig. 1A). In contrast to these emphases on reconsolidation enhancing memory stability, the present focus on memory updating does not require that reconsolidation has an endogenous part to play in the ongoing processing of a memory that requires no further modification. Indeed, the reverse may be suggested, in that a memory will persist in a stable and fixed form only if reconsolidation is not engaged, precisely because reconsolidation is the mechanistic instantiation of memory updating. Thus reconsolidation only plays a part in enhancing memory stability if such enhancement is dependent upon modification of the memory.

Rather than focussing on parametric factors in the constraint of reconsolidation, Morris et al. [36] argue for a mode-based explanation. Namely it may be the dual activation of retrieval and encoding states that drives reconsolidation processes. This model is well suited to account for situations in which new experiences result in profound changes to the memory; a change in the location of an escape platform in a water maze being the example used for the delayed non-mapping to place task [36]. However, it is not clear either how it may be adapted to conditions of more minor memory modifications (such as strength), or whether the activation of an “encoding mode” is sufficient to trigger reconsolidation. For example, extinction training clearly involves memory retrieval as well as new memory encoding, but under such circumstances reconsolidation is not obviously engaged [27, 50, 51, 53]. Moreover, the mode requirement appears to be an additional, rather than alternative, boundary condition to those discussed previously.


6. Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends Neurosci. 2005; 28:51–56. [PubMed: 15626497]

8. Dudai Y, Eisenberg M. Rites of passage of the engram: reconsolidation and the lingering consolidation hypothesis. Neuron. 2004; 44:93–100. [PubMed: 15450162]

27. Lee JLC, et al. Reconsolidation and extinction of conditioned fear: inhibition and potentiation. J Neurosci. 2006; 26:10051–10056. [PubMed: 17005868]

37. Rossato JI, et al. Retrieval induces hippocampal-dependent reconsolidation of spatial memory. Learn Mem. 2006; 13:431–440. [PubMed: 16882860]

50. Suzuki A, et al. Memory reconsolidation and extinction have distinct temporal and biochemical signatures. J Neurosci. 2004; 24:4787–4795. [PubMed: 15152039]

51. Pedreira ME, Maldonado H. Protein synthesis subserves reconsolidation or extinction depending on reminder duration. Neuron. 2003; 38:863–869. [PubMed: 12818173]

53. Eisenberg M, et al. Stability of retrieved memory: Inverse correlation with trace dominance. Science. 2003; 301:1102–1104. [PubMed: 12934010]

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However, this is not a universal finding, with contextual fear and appetitive cocaine-related memories showing reconsolidation up to a month following learning (Lee et al., 2006; Debiec et al., 2002). Nevertheless, it remains possible that all memories possess an age-dependent sensitivity to reconsolidation induced impairment, but with divergent time-courses thus far unaccounted for by the current literature. Alternatively, as suggested by Lee (2009), given that there is an interaction between memory age and the duration of stimulus re-exposure required to successfully reactivate a contextual fear memory (Suzuki et al., 2004), it is further possible that all memories undergo reconsolidation regardless of their age, but that previous studies have failed to employ sufficiently strong memory reactivation cues for older memories. However, as further purported by Lee, if the age of a memory does indeed represent a limit on the engagement of reconsolidation mechanisms, this might speculatively fit in with an updating hypothesis. Perhaps the passage of time, under certain circumstances, results in new experiences being more likely to be encoded separately from the original memory. As such it would be predicted that updating an old memory should engage consolidation specific mechanisms [e.g., brain-derived neurotrophic factor [BDNF] in the hippocampus for contextual fear memories (Lee et al., 2004)]. Moreover, selective interference with these mechanisms should only affect the new updating information, thereby resulting not in amnesia, as would be expected if reconsolidation mechanisms were being engaged and disrupted, but in a failure to modify the memory.

The issue concerning whether a new experience updates an existing memory trace or triggers new memory trace formation might also underlie the already established constraint that extinction places on reconsolidation. Memory reactivation protocols typically involve short extinction sessions. However, lengthier non-reinforced stimulus exposure reverses the impact of amnestic treatment.

However, this is by no means a universal finding, with contextual fear and appetitive cocaine-related memories reconsolidating up to a month after learning [42, 49]. Nevertheless, it remains possible that all memories do display an age-dependent sensitivity to reconsolidation impairment, but with different timecourses not yet revealed by the current literature. Alternatively, given that there is an interaction between memory age and duration of stimulus re-exposure required successfully to reactivate a contextual fear memory [50], it is also possible that all memories undergo reconsolidation regardless of their age, but that previous studies have failed to use sufficiently intense memory reactivation conditions for older memories. However, if the age of a memory does indeed represent a limit on the engagement of reconsolidation mechanisms, this might speculatively fit in with an updating hypothesis. Perhaps the passage of time, under certain circumstances, results in new experiences being more likely to be encoded separately from the original memory. A prediction of this view would be that updating an old memory should engage consolidation-specific mechanisms (e.g. BDNF in the hippocampus for contextual fear memories [22]). Moreover, selective interference with these mechanisms should affect only the new updating information, thus resulting not in amnesia, as would be expected if reconsolidation mechanisms were being engaged and disrupted, but in a failure to modify the memory.

The issue of whether a new experience updates an existing memory or triggers new memory formation may also underlie the established constraint that extinction places on reconsolidation. Memory reactivation protocols typically involve short extinction sessions. However, lengthier non-reinforced stimulus exposure reverses the impact of amnestic treatment.


22. Lee JLC, et al. Independent cellular processes for hippocampal memory consolidation and reconsolidation. Science. 2004; 304:839–843. [PubMed: 15073322]

42. Lee JLC, et al. Cue-induced cocaine seeking and relapse are reduced by disruption of drug memory reconsolidation. J Neurosci. 2006; 26:5881–5887. [PubMed: 16738229]

49. Debiec J, et al. Cellular and systems reconsolidation in the hippocampus. Neuron. 2002; 36:527– 538. [PubMed: 12408854]

50. Suzuki A, et al. Memory reconsolidation and extinction have distinct temporal and biochemical signatures. J Neurosci. 2004; 24:4787–4795. [PubMed: 15152039]

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The search for an endogenous function for the process of reconsolidation remains a fundamental issue. As noted by Dudai (2007), reconsolidation might not serve any function, particularly given the remote chance of encountering in everyday life the forms of agents used experimentally to induce amnesia. Nevertheless, interference is a potent cause of amnesia in reconsolidation studies (e.g., Walker et al., 2003; Hupbach et al., 2007) and stress can also be detrimental to reactivated memories (Maroun & Akirav, 2008; Wang et al., 2008), thereby suggesting that retrieval-induced plasticity places a memory trace at risk of disruption. As such, reconsolidation has been conceptualized as a fundamental process in the ongoing modification and storage of memories.

Indeed, it has often been suggested that reconsolidation might enable memories to be modified or updated (e.g., Tronson & Taylor, 2007; Dudai & Eisenberg, 2004; Sara, 2000). Generally, memories are retrieved in circumstances wherein additional complementary information is presented. As such, the capacity for plastic alterations in memory strength or content following memory retrieval would appear adaptive in terms of maintaining a memory’s relevance with respect to guiding future behaviour (Lee, 2009). Indeed, in terms of human episodic memories, interference congruent with retrieval of a prior memory results in an incorrectly updated memory for a list of items (Hupbach et al., 2007), thereby suggesting a role of reconsolidation in updating memories. However, Tronel and colleagues (2005), in a study adopting inhibitory avoidance learning in rats, did not find evidence that [reconsolidation is functionally involved in linking new information to a reactivated memory.]

[page 2]

While much has been learned regarding the mechanisms of reconsolidation, the search for an endogenous function of the process remains a fundamental issue. As noted by Dudai [11], reconsolidation might not serve any function, especially given the remote chance of encountering in real life the kinds of agents used experimentally to induce amnesia. Nevertheless, interference is a potent cause of amnesia in reconsolidation studies [12-14], and stress can also be detrimental to reactivated memories [15, 16], suggesting that retrieval-induced plasticity does place a memory genuinely at risk of disruption.

It has often been suggested that reconsolidation may enable memories to be modified or updated [5, 8, 9, 13, 17, 18]. Memories are retrieved often in situations presenting additional complementary information. Thus the capacity for plastic changes in memory strength or content following memory retrieval seems potentially adaptive in terms of maintaining a memory’s relevance in guiding future behaviour. [Three studies are of direct relevance to the hypothesis that reconsolidation mediates memory updating (see Box 1 for brief experimental details of the following tasks).] Firstly, in human episodic memories, interference congruent with retrieval of a prior memory results in an incorrectly updated memory for a list of items [13]. This finding is consistent with, though not directly demonstrative of, a role of reconsolidation in updating memories. Moreover, a prior study of inhibitory avoidance learning in rats did not provide evidence that reconsolidation is functionally involved in linking new information to a reactivated memory [19].

[page 6]

Thus reconsolidation may be viewed as a fundamental process in the ongoing modification and storage of memories.


5. Tronson NC, Taylor JR. Molecular mechanisms of memory reconsolidation. Nat Rev Neurosci. 2007; 8:262–275. [PubMed: 17342174]

8. Dudai Y, Eisenberg M. Rites of passage of the engram: reconsolidation and the lingering consolidation hypothesis. Neuron. 2004; 44:93–100. [PubMed: 15450162]

9. Sara SJ. Retrieval and reconsolidation: Toward a neurobiology of remembering. Learn Mem. 2000; 7:73–84. [PubMed: 10753974]

11. Dudai, Y. Post-activation state: a critical rite of passage of memories. In: Bontempi, B., et al., editors. Memories: Molecules and Circuits. Springer-Verlag; 2007. p. 69-82.

12. Walker MP, et al. Dissociable stages of human memory consolidation and reconsolidation. Nature. 2003; 425:616–620. [PubMed: 14534587]

13. Hupbach A, et al. Reconsolidation of episodic memories: A subtle reminder triggers integration of new information. Learn Mem. 2007; 14:47–53. [PubMed: 17202429]

14. Gordon WC, Feldman DT. Reactivation-induced interference in a short-term retention paradigm. Learn Motiv. 1978; 9:164–178.

15. Maroun M, Akirav I. Arousal and stress effects on consolidation and reconsolidation of recognition memory. Neuropsychopharmacology. 2008; 33:394–405. [PubMed: 17429409]

16. Wang XY, et al. Stress impairs reconsolidation of drug memory via glucocorticoid receptors in the basolateral amygdala. J Neurosci. 2008; 28:5602–5610. [PubMed: 18495894]

17. Dudai Y. The neurobiology of consolidations, or, how stable is the engram? Annu Rev Psychol. 2004; 55:51–86. [PubMed: 14744210]

18. Dudai Y. Reconsolidation: the advantage of being refocused. Curr Opin Neurobiol. 2006; 16:174– 178. [PubMed: 16563730]

19. Tronel S, et al. Linking new information to a reactivated memory requires consolidation and not reconsolidation mechanisms. PLoS Biol. 2005; 3:e293. [PubMed: 16104829]

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[If the assumption is made that NF-kB activity is reflective of a reconsolidation/updating process,] the extinction-induced inhibition would be consistent with a suppression of memory updating in favour of new extinction learning.

A further boundary condition on memory reconsolidation has recently been termed the ‘predictability of the reactivation stimulus’ (Nader & Hardt, 2009). This condition reflects findings emerging primarily from the crab literature that a mismatch between expected and actual events during reactivation triggers reconsolidation. Pedreira and colleagues (2004) found that reconsolidation only took place, and thus could only be disrupted, when the predictive context ended in the unexpected absence of the aversive outcome. It is not merely the case that memory reactivation must differ in some respect to conditioning, as there are numerous instances whereby reconsolidation impairments have been observed when the reactivation session is operationally identical to training (e.g., using reinforced reactivation procedures in fear conditioning (Eisenberg & Dudai, 2004; Duvarci & Nader, 2004), and in many (Kelly et al., 2003; Akirav & Maroun, 2006), but not all (Rossato et al., 2007) studies of object recognition memories). Instead, reconsolidation is triggered by a violation of expectation based upon prior learning, whether such a violation is qualitative (i.e., the outcome not occurring at all) or quantitative (i.e., the magnitude of the outcome not being fully predicted). It has thus been predicted that further initial training of fear or object memories would render such memories resistant to reconsolidation impairments through the use of reactivation sessions that are identical to training. Such an interpretation suggests that incompletely, but not fully, learned memories are subject to reconsolidation given the requirement for memory updating to optimize further the predictive accuracy of the memory.

Several hypotheses have been put forth regarding the role of reconsolidation in terms of wider memory processes. Two of these (Alberini, 2005; Dudai & Eisenberg, 2004) have adopted the temporal boundary condition to argue that reconsolidation plays a role in an extended process of memory stabilization.

[page 6]

If we make the assumption that NF-κB activity is reflective of a reconsolidation/updating process, the extinction-induced inhibition would be consistent with a suppression of memory updating in favour of new extinction learning.

A further boundary condition on memory reconsolidation has recently been termed the “predictability of the reactivation stimulus” [10]. This reflects the findings emerging primarily from the Chasmagnathus literature that a mismatch between expected and actual events during reactivation triggers reconsolidation. Pedreira et al. [56] found that reconsolidation only took place, and thus could only be disrupted, when the predictive context terminated in the unexpected absence of the aversive outcome. It is not simply that memory reactivation must differ in some manner to conditioning, as there are numerous instances where reconsolidation impairments have been observed when the reactivation session is operationally identical to training (e.g. using reinforced reactivation procedures in fear conditioning [48, 57], and in many [35, 58], but not all [59] studies of object recognition memories). Instead, reconsolidation is triggered by a violation of expectation based upon prior learning, whether such a violation is qualitative (the outcome not occurring at all) or quantitative (the magnitude of the outcome not being fully predicted). It is predicted, then, that more extended initial training of fear or object memories will render those memories resistant to reconsolidation impairments with the use of reactivation sessions that are identical to training. This interpretation, therefore, partially reduces to the prior discussion of memory strength, in that incompletely, but not fully, learned memories are subject to reconsolidation because of the requirement for memory updating in order to optimise further the predictive accuracy of the memory.

[page 7]

Several positions have been advanced regarding the role of reconsolidation in wider memory processes. Two of these [6, 8] have used the apparent temporal boundary condition to argue that reconsolidation plays a part in an extended process of memory stabilisation.


6. Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends Neurosci. 2005; 28:51–56. [PubMed: 15626497]

8. Dudai Y, Eisenberg M. Rites of passage of the engram: reconsolidation and the lingering consolidation hypothesis. Neuron. 2004; 44:93–100. [PubMed: 15450162]

10. Nader K, Hardt O. A Single Standard For Memory: The Case For Reconsolidation. Nature Reviews Neuroscience. 2009; 10:224–234.

35. Kelly A, et al. Activation of mitogen-activated protein kinase/extracellular signal-regulated kinase in hippocampal circuitry is required for consolidation and reconsolidation of recognition memory. J Neurosci. 2003; 23:5354–5360. [PubMed: 12832561]

48. Eisenberg M, Dudai Y. Reconsolidation of fresh, remote, and extinguished fear memory in medaka: old fears don’t die. Eur J Neurosci. 2004; 20:3397–3403. [PubMed: 15610172]

56. Pedreira ME, et al. Mismatch between what is expected and what actually occurs triggers memory reconsolidation or extinction. Learn Mem. 2004; 11:579–585. [PubMed: 15466312]

57. Duvarci S, Nader K. Characterization of fear memory reconsolidation. J Neurosci. 2004; 24:9269– 9275. [PubMed: 15496662]

58. Akirav I, Maroun M. Ventromedial prefrontal cortex is obligatory for consolidation and reconsolidation of object recognition memory. Cereb Cortex. 2006; 16:1759–1765. [PubMed: 16421330]

59. Rossato JI, et al. On the role of hippocampal protein synthesis in the consolidation and reconsolidation of object recognition memory. Learn Mem. 2007; 14:36–46. [PubMed: 17272651]

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[Therefore, in terms of contextual fear memories, protein] synthesis impairs reconsolidation in order to decrease fear when the context re-exposure is short, but conversely disrupts extinction in order to maintain high levels of fear when the duration of context re-exposure is more prolonged (Suzuki et al., 2004). Such a hypothesis has been replicated in cued fear memories (Lee et al., 2006) as well as in contextual aversive learning in the crab Chasmagnathus (Pedreira & Maldonado, 2003), although it appears that extinction does not always block reconsolidation from taking place (Duvarci et al., 2006). Thus, it is not merely the level of extinction training, but its relationship with initial learning that determines the interaction between reconsolidation and extinction. Protein synthesis inhibition during the same reactivation/extinction parameters has yielded opposing effects when the strength of initial training on a conditioned taste aversion task is varied (Eisenberg et al., 2003), which was conceptualised as a trace dominance process, whereby the dominant trace engaged by reactivation/extinction is that which is impacted upon by experimental treatment. However, instead of competition between traces, the extent of extinction training relative to conditioning may determine whether or not a new inhibitory memory is formed. Thus, if stimulus exposure is sufficient to engage extinction learning, this would not concomitantly modify the original excitatory memory. Alternatively, more limited exposure, would serve to trigger memory updating in the absence of new inhibitory learning. Providing support for such a contention is the recent finding in the crab that the transcription factor nuclear factor-kB (NF-kB) reflects a molecular switch between reconsolidation and extinction (Merlo & Romano, 2008). Inhibiting NFkB both impairs reconsolidation (Merlo et al., 2005) and enhances extinction (Merlo & Romano, 2008) under the appropriate conditions. Consequently, short memory reactivation induces a functional upregulation of NF-kB, whereas more prolonged extinction results in a functional inhibition. If the assumption is made that NF-kB activity is reflective of a reconsolidation/updating process, [the extinction-induced inhibition would be consistent with a suppression of memory updating in favour of new extinction learning.] [page 5]

Thus for contextual fear memories, protein synthesis impairs reconsolidation to reduce fear when the context re-exposure is short, but disrupts extinction to maintain high

[page 6]

levels of fear when the duration of context re-exposure is more prolonged [50]. This pattern of result has been replicated in cued fear memories [27] as well as in contextual aversive learning in the crab Chasmagnathus [51], though it appears that extinction does not always prevent reconsolidation from taking place [52]. It is not simply the level of extinction training, but its relation to initial learning, that governs the interaction between reconsolidation and extinction. Protein synthesis inhibition during the same reactivation/extinction parameters produced opposing effects when the strength of initial training on a conditioned taste aversion task was varied [53]. This has previously been conceptualised as a trace dominance process, whereby the dominant trace engaged by reactivation/extinction is that which is impacted upon by experimental treatment [53]. However, rather than appealing to competition between traces, the extent of extinction training relative to conditioning may determine whether or not a new inhibitory memory is formed. This argument states that if stimulus exposure is sufficient to engage extinction learning, this would not concomitantly modify the original excitatory memory. More limited exposure, by contrast, would trigger memory updating in the absence of new inhibitory learning. Perhaps in support of this interpretation is the recent finding in Chasmagnathus that the transcription factor NF-κB reflects a molecular switch between reconsolidation and extinction [54]. Inhibiting NF-κB both impairs reconsolidation [55] and enhances extinction [54] under the appropriate conditions. Consequently, short memory reactivation induces a functional upregulation of NF-κB, whereas more prolonged extinction results in a functional inhibition. If we make the assumption that NF-κB activity is reflective of a reconsolidation/updating process, the extinction-induced inhibition would be consistent with a suppression of memory updating in favour of new extinction learning.


27. Lee JLC, et al. Reconsolidation and extinction of conditioned fear: inhibition and potentiation. J Neurosci. 2006; 26:10051–10056. [PubMed: 17005868]

50. Suzuki A, et al. Memory reconsolidation and extinction have distinct temporal and biochemical signatures. J Neurosci. 2004; 24:4787–4795. [PubMed: 15152039]

51. Pedreira ME, Maldonado H. Protein synthesis subserves reconsolidation or extinction depending on reminder duration. Neuron. 2003; 38:863–869. [PubMed: 12818173]

52. Duvarci S, et al. Extinction is not a sufficient condition to prevent fear memories from undergoing reconsolidation in the basolateral amygdala. Eur J Neurosci. 2006; 24:249–260. [PubMed: 16882021]

53. Eisenberg M, et al. Stability of retrieved memory: Inverse correlation with trace dominance. Science. 2003; 301:1102–1104. [PubMed: 12934010]

54. Merlo E, Romano A. Memory extinction entails the inhibition of the transcription factor NFkappaB. PLoS ONE. 2008; 3:e3687. [PubMed: 18997870]

55. Merlo E, et al. Activation of the transcription factor NF-kappaB by retrieval is required for longterm memory reconsolidation. Learn Mem. 2005; 12:23–29. [PubMed: 15687229]

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[As such, reconsolidation is a neurobiologically distinct memory process, which is] increasingly associated with specific cellular mechanisms, such as the expression of the immediate-early gene zif268 (Lee et al., 2004, 2005).

The existence of reconsolidation processing is for the mostpart revealed by its absence. Quintessentially, when amnesia for a memory that is one or more days old is induced in a manner that is dependent upon the reactivation of said memory trace through retrieval, reconsolidation is considered to have been impaired (Nader et al., 2000; Dudai, 2004). However, similar to other cognitive functions, experimental treatments specifically aimed at targeting memory reconsolidation can also yield subsequent improvements (Tronson et al., 2006; Lee et al., 2006; Frenkel et al., 2005; Rodriguez et al., 1999; Blaiss & Janak, 2006). Further, the possibility to improve a memory trace through post-retrieval processing infers a potentially adaptive function for the reconsolidation process. Thus, instead of merely being process that restabilizes a memory following its retrieval, reconsolidation also represents a special state which allows for renewed memory plasticity and modulation (Dudai, 2007). Importantly, such memory-enhancing interventions include naturalistic phenomena such as water deprivation and the administration of glucose (Frenkel et al., 2005; Blaiss & Janak, 2006). Therefore, the ability to modify (e.g., strengthen) a previously acquired memory in a potentially adaptive manner is not limited to exogenous pharmacological treatment but is likely to be relevant to naturalistic situations of memory updating.

However, even in paradigms with well-established demonstrations of reactivation-dependent amnesia, there are conditions under which reconsolidation does not take place. Therefore, there exist certain boundary conditions around which reconsolidation may or may not be observed. First, temporal dynamics play an important role. In inhibitory avoidance in rats (Milekic & Alberini, 2002), as well as in fear conditioning in the medaka fish (Eisenberg & Dudai, 2004), 14-day-old memories did not demonstrate reactivation-dependent amnesia, [whereas younger memories did show evidence of reconsolidating.]

[page 3]

Therefore, reconsolidation is a neurobiologically-distinct memory process, which is beginning to be associated with specific cellular mechanisms, such as the expression of the immediate-early gene zif268 [22, 25].

The existence of a reconsolidation process is largely revealed by its absence. Typically, when amnesia for a memory that is one or more days old is induced in a manner that is dependent upon reactivation of that memory through retrieval, reconsolidation is said to have been impaired [4, 17]. However, in common with other cognitive functions, experimental treatments targeting memory reconsolidation can also result in subsequent improvements [26-30]. Gain-of-function findings are of particular importance in refuting non-specific accounts of amnesia. Moreover, the ability to improve a memory through postretrieval processing suggests a potentially adaptive function for the reconsolidation process. Rather than simply being process that restabilises a memory following its retrieval, it represents a special state, providing an opportunity for renewed memory plasticity and modulation [11]. Notably, the aforementioned memory-enhancing interventions include naturalistic phenomena such as water deprivation and the administration of glucose [28, 29]. Therefore, the capacity to modify (e.g. strengthen) a previously-acquired memory in a potentially adaptive manner is not limited to exogenous pharmacological treatment, but is likely also to be relevant to naturalistic situations of memory updating.

[page 5]

Even in paradigms with well-established demonstrations of reactivation-dependent amnesia, there are conditions under which reconsolidation does not take place. Therefore, there exist certain boundary conditions, which for the purposes of this review, are considered simply to be a description of the boundaries around which reconsolidation may or may not be observed. [...]

Other than the impact of memory strength, several boundary conditions exist. The first among these is temporal in nature. In inhibitory avoidance in rats [47], as well as in fear conditioning in the medaka fish [48], 14-day old memories did not display reactivationdependent amnesia, whereas younger memories did show evidence of reconsolidating.


4. Nader K, et al. Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature. 2000; 406:722–726. [PubMed: 10963596]

11. Dudai, Y. Post-activation state: a critical rite of passage of memories. In: Bontempi, B., et al., editors. Memories: Molecules and Circuits. Springer-Verlag; 2007. p. 69-82.

17. Dudai Y. The neurobiology of consolidations, or, how stable is the engram? Annu Rev Psychol. 2004; 55:51–86. [PubMed: 14744210]

22. Lee JLC, et al. Independent cellular processes for hippocampal memory consolidation and reconsolidation. Science. 2004; 304:839–843. [PubMed: 15073322]

25. Lee JLC, et al. Disrupting reconsolidation of drug memories reduces cocaine seeking behavior. Neuron. 2005; 47:795–801. [PubMed: 16157275]

26. Tronson NC, et al. Bidirectional behavioral plasticity of memory reconsolidation depends on amygdalar protein kinase A. Nat Neurosci. 2006; 9:167–169. [PubMed: 16415868]

27. Lee JLC, et al. Reconsolidation and extinction of conditioned fear: inhibition and potentiation. J Neurosci. 2006; 26:10051–10056. [PubMed: 17005868]

28. Frenkel L, et al. Memory strengthening by a real-life episode during reconsolidation: an outcome of water deprivation via brain angiotensin II. Eur J Neurosci. 2005; 22:1757–1766. [PubMed: 16197516]

29. Rodriguez WA, et al. Effects of glucose and fructose on recently reactivated and recently acquired memories. Prog Neuropsychopharmacol Biol Psychiatry. 1999; 23:1285–1317. [PubMed: 10581649]

30. Blaiss CA, Janak PH. Post-training and post-reactivation administration of amphetamine enhances morphine conditioned place preference. Behav Brain Res. 2006

47. Milekic MH, Alberini CM. Temporally Graded Requirement for Protein Synthesis following Memory Reactivation. Neuron. 2002; 36:521–525. [PubMed: 12408853]

48. Eisenberg M, Dudai Y. Reconsolidation of fresh, remote, and extinguished fear memory in medaka: old fears don’t die. Eur J Neurosci. 2004; 20:3397–3403. [PubMed: 15610172]

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Recognition memory is a well-studied example of declarative memory and depends on the integrity of the medial temporal lobe and diencephalic structures (Reed & Squire, 1997; Manns & Squire, 1999). In the VPA task (Fantz, 1964; Fagan, 1970), two identical pictures are presented side by side for a brief viewing period (e.g., 5 sec). After a delay (e.g., 5 minutes; 24 hours), one of the previously viewed pictures is presented along with a new picture. The phenomenon of interest is that individuals will look more at the novel picture than the familiar picture. On the one hand, the task has many of the features of implicit memory. No reference is made to a study episode, and performance appears to have an automatic quality that is reminiscent of habituation. [In fact, the task is commonly used to assess memory in infants who would certainly not yet understand any explicit instructions even if given (Fagan, 1970).] On the other hand however, the direction of gaze is voluntary, and a preference for the new picture could be guided by the same recollective processes that support recognition memory (Manns et al., 2000). More specifically, in humans, Manns and colleagues (2000) found that performance on the VPA task was predictive of subsequent recognition memory performance whereas perceptual priming was unrelated to subsequent recognition memory performance. These results are consistent with the data from lesion studies and suggest that performance on the VPA task measures a form of declarative memory. We found that performance on the visual paired-comparison task was predictive of subsequent recognition memory performance whereas perceptual priming was unrelated to subsequent recognition memory performance. The results are consistent with the data from lesions and suggest that performance on the visual paired-comparison task measures a form of declarative memory.

[...]

In contrast to perceptual priming, recognition memory is a well-studied example of declarative memory and depends on the integrity of the medial temporal lobe and diencephalic structures (17, 18). [...]

[...] For example, in the visual paired-comparison task (27, 28), two identical pictures are presented side by side for a brief viewing period (e.g., 5 sec). After a delay (e.g., 5 min), one of the previously viewed pictures is presented along with a new picture. The phenomenon of interest is that individuals will look more at the new picture than the old picture. The question naturally arises: What kind of memory is being exhibited in the visual paired-comparison task? On the one hand, the task has many of the features of implicit memory. No reference is made to a study episode, and performance appears to have an automatic quality that is reminiscent of habituation. On the other hand, the direction of gaze is voluntary, and a preference for the new picture could be guided by the same recollective processes that support recognition memory.


17. Reed, J. M. & Squire, L. R. (1997) Behav. Neurosci. 111, 667–675.

18. Manns, J. R. & Squire, L. R. (1999) Hippocampus 9, 495–499.

27. Fantz, R. L. (1964) Science 146, 668–670.

28. Fagan, J. F. (1970) J. Exp. Child Psychol. 9, 217–226.

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A reference to the source is given (twice in the documented text, and once before it), but the amount of text taken from the source (including 4 references to the literature) is not clear to the reader.

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The majority of research into contextual binding between objects and context stems primarily from studies conducted on object perception or object identification in humans, which has typically shown that contextual information enhances object identification (Palmer, 1975; Biederman et al., 1982; Boyce & Pollatsek, 1992; Davenport & Potter, 2004). [Such experiments focused on pre-existing, semantic relationships between objects and their associated contexts.] For example, Bar and Ullman (1996) showed that the presence of a clearly identifiable object facilitated identification of an ambiguous object when the identifiable object was semantically related, as did the presentation of realistic spatial relationships between related objects. However, the implicit influence of visual context on memory for specific, episodically-mediated abstract paired-associates remains to be elucidated (however see Hayes, Nadel & Ryan, 2007 for episodic object recognition).

Neuroimaging studies of scene processing (Epstein & Kanwisher, 1998), object identification (Bar & Aminoff, 2003), and intentional retrieval of visual context information (Hayes et al., 2004) suggest that the medial temporal lobes, most likely the parahippocampal cortex (PHC), may be involved in visual context effects mediating episodic object recognition. Indeed, Hayes and colleagues (2007) recently found that the PHC is important not only for processing of scene information, but also plays a role in successful episodic memory encoding and retrieval.

The results suggest that PHC is important not only for processing of scene information, but also plays a role in successful episodic memory encoding and retrieval.

[page 2]

Evidence for the role of context in object memory comes primarily from research on object perception or object identification in humans, which has shown that contextual information enhances object identification (Palmer, 1975; Biederman et al., 1982; Boyce and Pollatsek, 1992; Davenport and Potter, 2004). For example, Bar and Ullman (1996) showed that the presence of a clearly identifiable object facilitated identification of an ambiguous object when the identifiable object was semantically related, as did the presentation of realistic spatial relationships between related objects.

[page 3]

However, the influence of visual context on memory for a specific, episodically presented object remains to be determined. [...]

[...]

[...] Neuroimaging studies of scene processing (Epstein and Kanwisher, 1998), object identification (Bar and Aminoff, 2003), and intentional retrieval of visual context information (Hayes et al., 2004) suggest that the medial temporal lobes, most likely the PHC, may be involved in visual context effects

[page 4]

mediating episodic object recognition[, although no study we are aware of has directly addressed this issue].

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Previous neuroimaging studies of scene processing, object identification, and intentional retrieval of visual context information suggest that the medial temporal lobes, most likely the parahippocampal cortex (PHC), may be involved in visual context effects mediating episodic object recognition. Hayes, Nadel and Ryan (2007) recently found that the PHC is important not only for processing of scene information, but also plays a role in successful episodic memory encoding and retrieval. [page 1]

[...] the results suggest that PHC is important not only for processing of scene information, but also plays a role in successful episodic memory encoding and retrieval.

[page 3]

Neuroimaging studies of scene processing (Epstein and Kanwisher, 1998), object identification (Bar and Aminoff, 2003), and intentional retrieval of visual context information (Hayes et al., 2004) suggest that the medial temporal lobes, most likely the PHC, may be involved in visual context effects

[page 4]

mediating episodic object recognition[, although no study we are aware of has directly addressed this issue].

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The source is mentioned, but it is not clear to the reader that the overview before that has also been taken from the source.

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[That these conditions are effective is hardly] surprising since the previous study had shown that context alone is enough to trigger updating.

This set of experiments demonstrates that reconsolidation, as reflected in memory updating effects dependent upon reminding, can be observed in human learning. They further show that such updating only occurs when the context is part of the reminder manipulation, at least in the experimental conditions of these aforementioned studies. Nadel and colleagues conjecture that these results support the idea that context plays a unique role in determining how the memory system behaves. Thus, when in the same context – updating and transformation of an existing memory trace ensues, but when in a new context, an entirely new memory representation is formed.

Thus, it appears that context is an integral component of episodic memory. It is, however, more than just a component of such memory. It also seems to play a determining role in the dynamics of the episodic memory system as a whole. To the extent to which this is the case, further study concerning how context is represented physiologically should greatly enhance our understanding of human memory.

That these conditions are effective is hardly surprising since the previous study had shown that context alone is enough to trigger updating.

This set of experiments demonstrates that reconsolidation, as reflected in memory updating effects dependent upon reminding, can be observed in human learning. They further show that such updating only occurs when the context is part of the reminder manipulation, at least in the experimental conditions of our studies. We believe these results support the idea that context plays a unique role in determining how the memory system behaves. Put most directly: when in the same context, an existing representation is updated and transformed, but when the organism is in a new context, an entirely new representation is created.

CONCLUSIONS

Context is a critical component of episodic memory. It is, however, more than just a component of such memory. It also seems to play a determining role in the dynamics of the episodic memory system as a whole. To the extent to which this is the case, further study of how context is represented physiologically should greatly enhance our understanding of human memory.

Anmerkungen

While it is clear to the reader that the first two paragraphs are describing the work of Nadel et al. the third paragraph is presented to the reader as a conclusion of the author.

That the structure of all three paragraphs as well as many formulations are taken from Nadel (2008) is not clear to the reader at all.

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Further, the majority of context-dependent research has been conducted in one of only two environmental or global contexts, subsequently testing memory retrieval in either in the same or an alternate environmental context.

Other contextual manipulations have focused on more local aspects of visual context combined with predominantly verbal materials, such as text colour, background color, or font. Dulsky (1935), in a series of experiments, reported a decrease in memory performance when the background colour of target nonsense syllables changed between study and test. Since then, many experiments have demonstrated decreased retrieval performance with changes between encoding and retrieval in the local verbal context (Tulving & Osler, 1968; Light & Carter-Sobell, 1970), font format and orientation (Graf & Ryan, 1990), background colour (Mori & Graf, 1996), or foreground and background colour (Dougal & Rotello, 1999). In a comprehensive series of experiments, Murnane and Phelps (1993, 1994, 1995) manipulated context by changing foreground (colour of the word), background (colour of computer screen), and the location of the word (upper left, lower right, and so on). In multiple experiments, a context shift decrement (i.e., decreased memory for items presented in different contexts at study and test) was observed. The context shift decrement was significantly enhanced when the words were originally studied in a visually rich context (computer-generated virtual reality scenes, such as on a chalkboard in a classroom) relative to simple visual contexts (coloured font, coloured background), or in various locations on the computer screen (Murnane et al., 1999).

The aforementioned experiments presented verbal materials in one of only two environmental or global contexts (underwater or on land), and then memory was tested either in the same or the alternate environmental context.

Other contextual manipulations have focused on more local aspects of visual context combined with verbal materials, such as text color, background color, or font. Dulsky (1935), in an elegant series of experiments, reported a decrease in memory performance when the background color of target nonsense syllables changed between study and test. Since then, many experiments have demonstrated decreased memory performance with changes between encoding and retrieval in the local verbal context (Tulving and Osler, 1968; Light and Carter-Sobell, 1970), font format and orientation (Graf and Ryan, 1990), background color (Mori and Graf, 1996), or foreground and background color (Dougal and Rotello, 1999). In a comprehensive series of experiments, Murnane and Phelps (1993, 1994, 1995) manipulated context by changing foreground (color of the word), background (color of computer screen), and the location of the word (upper left, lower right, etc.). In multiple experiments, a context shift decrement (CSD) — decreased memory for items presented in different contexts at study and test was — observed. The CSD was significantly enhanced when the words were originally studied in a visually rich context (computer-generated virtual reality scenes, such as on a chalkboard in a classroom) relative to simple visual contexts (colored font, colored background, or in various locations on the computer screen; Murnane et al., 1999).

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Unstimulated (i.e., presumably unaffected by stressors or other factors – ‘normal’/baseline level) cortisol follows a diurnal rhythm that is dictated by the sleep-wake cycle, rather than a light-dark cycle: there is a typical and consistent flood of cortisol in the body upon awakening, generally declining thereafter, and cortisol secretion follows a series of peaks and troughs throughout the day, [with a small peak associated with a lunch-time meal (Preussner et al., 1997, in Pollard & Ice, 2007; Kirschbaum & Hellhammer, 2000),] which tends to taper off to a more steady, less steep decline in the afternoon. It is for this reason that laboratory studies examining cortisol generally schedule post-noon testing sessions. [Therefore, all participants were scheduled to commence the session at 3pm in the current study (see Appendix 14).] Variations in this cycle are seen in clinical populations – for instance, a blunted response has been demonstrated in individuals with depression and those experiencing socioeconomic hardship, while extremely elevated, or again, blunted cortisol release can result from a variety of medical conditions. Cortisol secretion can be affected by everyday factors such as consumption of food or beverages prior to sampling, or disrupted sleep patterns. [As a result, stringent guidelines were set forth to control for these factors, and various control measures were distributed (see above) to screen for possible psychopathologies (see Appendices 10 and 11).]

Cortisol in saliva is a particularly robust biologically-active compound, and samples remain viable for several days at room temperature, as well as when frozen and refrozen.

Unstimulated (i.e., presumably unaffected by stressors or other factors – ‘normal’/baseline level) cortisol follows a diurnal rhythm that is dictated by the sleep-wake cycle, rather than a light-dark cycle: there is a typical and consistent flood of cortisol in the body upon awakening, generally declining thereafter, and cortisol secretion follows a series of peaks and troughs throughout the day, which tend to taper off to a more steady, less steep decline in the afternoon. It is for this reason that laboratory studies examining cortisol usually schedule post-noon testing sessions. Variations in this cycle are seen in clinical populations – for instance, a blunted response has been demonstrated in individuals with depression and those experiencing socioeconomic hardship, while extremely elevated, or again, blunted cortisol release can result from a variety of medical conditions. Cortisol secretion can be affected by everyday factors such as consumption of food or beverages prior to sampling, or disrupted sleep patterns. [Clinically, hyper-secretion of cortisol can lead to the development of Cushing’s disease. while hypo-secretion can result in Addison’s disease.]

Cortisol in saliva is a particularly robust biologically-active compound, and samples remain viable for several days at room temperature, as well as when frozen and refrozen.

Anmerkungen

No source is given.

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[Nadel and colleagues] interpreted these results as indicative that the reminder presented prior to List 2 learning reactivated the memory trace for List 1, and thereby triggered an “update” mechanism which caused the subject to confuse the List 2 and List 1 objects. In the absence of the reminder, the subjects treated List 2 learning and List 1 learning as separate episodes and intrusions did not occur.

This research team, more recently, has begun to explore exactly what kinds of reminders play a critical role in initiating this “update” mechanism (Hupbach et al., 2008). In the original study the reminder involved returning the subject back to the same context, with the same Experimenter, who asked a leading question about the List 1 training experience. The no-reminder group was brought to a different context, with a different Experimenter, and was not asked about List 1 training. In the most recent of such work, these authors systematically manipulated the nature of the “reminders” available to the subjects prior to learning List 2. In one set of studies, only one of the three reminder cues was presented: the original training context, the original Experimenter, or the leading question about the basket in which List 1 objects were kept. Results revealed that only the group that received a context reminder showed the memory updating effect. The other two groups showed few if any intrusions of List 2 items into List 1 memory, thereby indicating that updating had not occurred in these groups.

Furthermore, in a second set of studies, two of the three cues were provided, either context plus Experimenter, context plus question, or Experimenter plus question, with the intention of investigating the possibility that the failure of the Experimenter or Question to initiate an updating process might have reflected that fact that these are weak cues compared to context, and that by combining these two weaker cues, updating would be demonstrated. Once again, only the provision of a context reminder, in combination with either the Experimenter or the Question, elicited updating.

[page 10]

We interpret these results as showing that the reminder prior to list 2 learning reactivates the memory of list 1, and triggers an “update” mechanism that causes the subject to conflate the list 2 and list 1 objects. Absent the reminder the subjects treat list 2 learning and list 1 learning as separate episodes and intrusions do not occur.

We have more recently started to explore exactly what kinds of reminders play a critical role in initiating this “update” mechanism (Hupbach et al., submitted). In the original study the reminder involved bringing the subject back to the same context, with the same experimenter, who asked a leading question about the list 1 training experience. The no-reminder group was

[page 11]

brought to a different context, with a different experimenter, and was not asked about list 1 training.

In our most recent work we systematically manipulated the nature of the “reminders” available to the subjects prior to learning list 2. In one set of studies we provided only one of the three reminder cues: the original training context, the original experimenter, or the leading question about the basket in which list 1 objects were kept. Figure 1-2A shows the results of these manipulations: only the group that received a context reminder showed the memory updating effect. The other two groups showed few if any intrusions of list 2 items into list 1 memory, indicating that updating had not occurred in these groups.

In a second set of studies we provided two of the three cues, either context plus experimenter, context plus question, or experimenter plus question. We wanted to explore the possibility that the failure of the Experimenter or Question to initiate an updating process might have reflected the fact that these are weak cues compared to context, and that by combining these two weaker cues we would be able to demonstrate updating. Figure 1-2B shows that this was not the case. Once again, only the provision of a context reminder, in combination with either the Experimenter or the Question, elicited updating.

Anmerkungen

It is clear from the text that here the work of Nadel et al. is described. It is not clear to the reader at all, that this description follows the structure and many formulations of Nadel (2008).

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[When subsequently asked to recall the event quite often the] misinformation rather than the original detail is remembered. One thing that distinguishes this work on human memory from the animal work discussed previously is the absence of any systematic manipulation of specific reminders.

With the intention of merging these two animal and human based findings, Nadel and colleagues recently developed a paradigm to study reconsolidation in human episodic memory that depends upon reminding subjects about what they previously learned (Hupbach et al., 2007). In this paradigm, subjects are initially trained on a “list” of objects. These everyday objects are kept in a blue basket and presented one by one to the subject. After all 20 objects are presented, the subject is asked to verbally “recall” the list. This training sequence is continued until the subject recalls at least 18 of the 20 objects (in any sequence). Typically this takes fewer than four training trials. Two days later subjects return to the laboratory and are divided into two groups. Subjects in one group are reminded of their previous training experience, whereas subjects in the other group are not. Subsequently, a second “list” of objects is learned, albeit in a different manner. The objects on this second list are laid out on a table instead of being contained in a basket. Following the learning of this second list recall for both lists is tested either immediately or two days later. In one study, recall of List 1 was tested first, followed by List 2, and in another study recall of List 2 was tested first, followed by List 1. In both studies retrieval performance of subjects that had been reminded was contrasted with subjects that had not.

The results emanating from this research stream can be summarized as follows (see Hupbach et al., 2007 for a more detailed account): if, and only if, a reminder was given prior to the learning of List 2, subjects inter-mixed items from List 2 into List 1 when asked to recall List 1. In another study these authors showed that this result is found only when recall is tested 2 days later. Intrusions from List 1 into List 2 recall were never observed, whether List 2 is recalled first or second, immediately or 2 days later.

[page 9]

When subsequently asked to recall the event quite often the misinformation rather than the original detail is remembered. One thing that distinguishes this important work on human memory from the animal work just discussed is the absence of any systematic manipulation of specific reminders.

In the hope of bringing these literatures together we have recently developed a paradigm to study reconsolidation in human episodic memory that depends on reminding the subjects about what they previously learned (Hupbach et al., 2007). Subjects are initially trained on a “list” of objects. These objects -- such things as a pencil, comb, or other similarly sized common object -- are kept in a blue basket and presented one by one to the subject. After all 20 objects are presented the subject is asked to verbally “recall” the

[page 10]

list. This training sequence is continued until the subject recalls at least 17 of the 20 objects (in any order) or for a maximum of four learning trials.

Two days later subjects return to the laboratory and are divided into two groups. Subjects in one group are reminded of their previous training experience, subjects in the other group are not. Then, a second “list” of objects is learned, but in a different way. The objects on this second list are arrayed on a table instead of being contained in a basket. Following the learning of this second list we test for recall of both lists either immediately or 2 days later. In one study we tested recall of list 1 and in another study we tested recall of list 2. In both studies we contrasted subjects twho had been reminded with subjects who had not.

The results can be summarized as follows (see Hupbach et al., for a full description of this study): if, and only if, a reminder is given prior to the learning of list 2, subjects will “intrude” items from list 2 into list 1 when asked to recall list 1 (Fig. 1-1A). Additionally we showed that this result occurs only when recall is tested 2 days later (Fig. 1- 1B). It is not observed when recall is tested immediately. Intrusions from list 1 into list 2 recall are never seen, regardless of whether list 2 is recalled immediately or second, immediately or 2 days later (see Fig. 1-1C).

Anmerkungen

It is clear from the text that the work of Nadel et al. is described here. It is not clear from the text, however, that this is done following the same structure and many formulations of Nadel (2008).

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[40.] Jm/Fragment 015 09 - Diskussion
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Although there is general consensus stipulating that the hippocampus plays a role in context effects (e.g., see Smith & Mizumori, 2006; Rudy et al., 2004; Gerwitz et al., 2000), a lack of cohesion arises concerning the nature of context itself, in particular the fact that there are multiple forms, and hence representations, of context, only one of which depends upon the hippocampus. [Nadel and Willner (1980) have argued that context representations formed in the hippocampus are essentially configural, being based on relations among the environmental features that comprise the physical lay-out of space. The authors further argued that because of this configural nature, learning about spatial context diverges in important respects from learning about isolated cues, or elements, within an environmental context. The authors further asserted that hippocampal damage would manifest as a lack of context-specificity, in the respect that learning should theoretically be inappropriately generalized to novel contexts.] [page 3]

[We argued that context representations formed in the hippocampus were fundamentally configural, being based on relations among the environmental features that comprised the physical lay-out of space. We further argued that because of this configural nature, learning about spatial context was different in important ways from learning about isolated cues, or elements, in the organism’s world2. [...]

A second idea we emphasized was that hippocampal damage would manifest as a lack of context specificity – learning would be inappropriately generalized to novel contexts.]

[page 4]

Although there is general agreement that the hippocampus plays a role in context effects, confusion arises from continued misunderstanding of the nature of context itself, in particular the fact that there are multiple forms, and hence representations, of context, only one of which depends upon the hippocampus.


[2 [...]]

Anmerkungen

Starting from the 2nd sentence it is clear that results of Nadel and Willner (1980) are presented. One might ask whether this presentation is not also taken from the source, but for the purpose here, only the first sentence is counted.

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[41.] Jm/Fragment 025 01 - Diskussion
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[Thus began a long tradition of linking what has] come to be termed systems-level memory consolidation to a shift from hippocampal to neocortical dominance in memory retrieval. The consolidation period was assumed to end when the hippocampal system was no longer essential in retrieval.

It was within this context that the concept of memory reconsolidation first emerged. A number of investigators in the 1960s and 1970s, unconvinced by the concept of consolidation, argued instead that memories were always open to alteration and/or disruption as long as they were in an active state (Lewis, 1979; Misanin et al., 1968). Memories could be reconverted into an active state through “reminders” such as exposing the organism to the CS used in the learning task, or the context in which learning took place. These ideas, though supported by several well-replicated findings, were neglected in favour of consolidation.

The notion of reconsolidation re-emerged in two labs: Sara and colleagues (e.g., Przybyslawski & Sara., 1997; Sara, 2000) and Nader, LeDoux and their colleagues (Nader et al., 2000) which both demonstrated that reminders could return well-consolidated memories for maze learning and fear conditioning, respectively, back to a fragile, labile state, and that these newly-fragile memories could be disrupted by the systemic injection of MK-801 (an NMDA channel blocker), or protein synthesis inhibitors into the amygdala, respectively. There followed a proliferation of studies demonstrating the robust nature of ‘reconsolidation’, its presence in a wide variety of species and learning situations, how it is differentiated from consolidation, and what some of the boundary conditions are that constrain it (refer to Moore & Roche, 2007, for a comprehensive account of the literature).

In a similar vein, a tradition of research using human subjects has demonstrated seemingly similar malleability in what should have been consolidated episodically mediated memories (e.g., Loftus, 2005). Much of this research employs a standard procedure wherein subjects are exposed to a complex event, and are later given misinformation concerning some detail of that event.

Thus began a long tradition of linking what has come to be called "systems-level memory consolidation" to a shift from hippocampal to neocortical dominance in memory retrieval. The consolidation period was assumed to end when the hippocampal system was no longer essential in retrieval.

It was in this context that the idea of memory reconsolidation first emerged. A number of investigators in the 1960s and 1970s, unconvinced by the consolidation idea, argued instead that memories were always open to alteration and/or disruption so long as they were in an active state (see Misanin et al., 1968, Lewis, 1979). Memories could be brought back to an active state through “reminders” such as exposing the organism to the CS used in the learning task, or the context in which learning took place. These ideas, though backed by several well-replicated findings, were pushed aside by the consolidation bandwagon[, for reasons that would be of interest in an article on the history of science, but that are beyond the scope of this effort.]

The notion of reconsolidation re-emerged in two labs: Sara and her colleagues (Przybyslawski and Sara, 1997; Sara, 2000) and Nader, LeDoux and their colleagues (Nader et al., 2000) showed that reminders could bring well-consolidated memories for maze learning and fear conditioning, respectively, back to a fragile state, and that these newly-fragile memories could be disrupted by the systemic injection of MK-801 (an NMDA receptor antagonist), or protein synthesis inhibitors into the amygdala, respectively. There has followed a torrent of studies demonstrating the robust nature of reconsolidation, its presence in a wide variety of species and learning situations, the ways in which it is differentiated from consolidation, and some of the boundary conditions that constrain it. [...]

At the same time, a tradition of research using human subjects has demonstrated apparently similar malleability in supposedly consolidated memories (see Loftus, 2005). Much of this work uses a standard procedure: subjects are exposed to a complex event, then some time later they are given misinformation about some detail of that event.

Anmerkungen

The source is not referenced.

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[As proposed by Nadel and colleagues above, after some weeks during which a rat is] not returned to the training context, its configural representation of that context weakens, and elemental contextual representations take over. In the absence of reminders that bring the context back into the frame, hippocampal lesions yield little or no effect. However, as various investigators (e.g., Debiec et al., 2002; Land et al., 2000) have reported in the reconsolidation literature; if animals are reminded of the context before lesions are made, then these lesions subsequently serve to impair retention.

Creating an entirely new representation in response to deciding that one is in a new environment differs from updating an existing representation based on some local change (Nadel, 2008). According to Nadel, this assertion is fundamental to the distinction between memory “consolidation” and memory “reconsolidation”. It has long been assumed that a time-dependent stabilization process unfolds after the initial acquisition of a memory (Müller & Pilzecker, 1900). During this time period, termed the “consolidation” interval, memories can be disrupted by new learning experiences, cerebral trauma, hypothermia, electroconvulsive shock, and so on. This idea was initially framed within both physiological and psychological terms, and included the possibility that the content of the memory might itself be transformed during consolidation (Burnham, 1903). Hebb (1949) isolated the physiological process underlying consolidation, thereby providing a comprehensive understanding concerning how exactly memories become stabilized. Hebb assumed that memories are isolated in the brain through changes in synaptic efficacy, and that these changes depend upon complex cellular and molecular mechanisms that lead to structural alterations underpinning potentiated synaptic function. According to Hebb these changes unfolded within the same cell assemblies initially activated by the experience, possibly through reverberations within these assemblies. Study of patient H.M., however, suggested that, in terms of memory for life’s episodes, consolidation involves a shift wherein brain structures are critical for memory retrieval.

[page 6]

As we argued above, after some weeks during which a rat is not returned to the training context, its configural representation of that context weakens, and elemental contextual representations take over. In the absence of reminders that bring the context back into the picture, hippocampal lesions have little or no effect. But, as Land et al., (2000) have shown, if animals are reminded of the context before lesions are made, these lesions can impair retention (for a similar result see Debiec et al., 2002).

[page 9]

Creating an entirely new representation in response to deciding that one is in a new environment is quite different than updating an existing representation on the basis of some local change. I believe this difference is fundamental to the distinction between memory “consolidation” and memory “reconsolidation”. [...]

It has long been assumed that a time-dependent stabilization process unfolds after initial acquisition of a memory (Muller and Pilzecker, 1900). During this time period, termed the “consolidation” interval, memories can be disrupted by new learning experiences, blows to the head, hypothermia, electroconvulsive shock, etc. This idea was initially couched in both physiological and psychological terms, and included the possibility that the content of the memory might itself be transformed during consolidation (cf., Burnham, 1903). Although these early writers assumed that consolidation involved a physiological process, the first detailed proposal came from Hebb (1949), who provided a way of understanding how memories could become stabilized. Hebb assumed that memories are captured in the brain through changes in synaptic efficacy, and that these changes depend upon complex cellular and molecular mechanisms that lead to structural alterations underpinning potentiated synaptic function. In Hebb’s view these changes unfolded within the same cell assemblies initially activated by the experience, possibly through reverberations within these assemblies. Study of patient H.M. (Scoville and Milner, 1957), however, suggested that, at least for episodic memory, consolidation involves a shift in which brain structures are critical for memory retrieval.

Anmerkungen

The source is referenced, but is not clear for the reader that the entire page is taken from it including various references to older literature.

The phrase "As proposed by Nadel and colleagues above" seems odd in a thesis by another author.

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[43.] Jm/Fragment 023 20 - Diskussion
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1.2.4 Context Recognition- The Key to Reconsolidation

[Context plays an integral role in the consolidation of a memory trace.] The impact of hippocampal lesions on the retention of a context-based task depend upon when retention is tested, and upon whether or not the animal was reminded of the context before retention was tested.

[page 6]

The impact of hippocampal lesions on retention of a context-based task will depend on when retention is tested, and on whether or not the animal was reminded of the context before retention was tested.

[page 9]

CONTEXT RECOGNITION – THE KEY TO RECONSOLIDATION

Anmerkungen

Beginning of a longer passage copied from Nadel (2008). See: Jm/Fragment_024_01

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[Paradoxically, animals with hippocampal lesions should theoretically be less] affected by such a shift than intact animals. In the case of conditioned fear, for example, hippocampally-lesioned rats should show greater-than-normal fear in an out-of-context test. Indeed, Nadel (1968) demonstrated this effect; rats with dorsal hippocampal lesions tested in context B for fear of a CS paired with shock in context A actually showed more fear than did control rats. This parallels observations of Penick and Solomon (1991), and is consistent with the report by Good and Honey (1991) showing that hippocampal lesions impaired rats’ ability to learn that a stimulus was reinforced in one context but not in another (see also Lehmann et al., 2005; but see Hall et al., 1996). It is also consistent with the recent findings that hippocampal inactivation impairs the context specificity of latent inhibition (Maren & Holt, 2000), and extinction (Corcoran et al., 2005; Hobin et al., 2006), and that reinstatement of conditioned fear in humans is context specific (LaBar & Phelps, 2005). Paradoxically, animals with hippocampal lesions should be less affected by such a shift than intact animals. In the case of conditioned fear, for example, hippocampal-lesioned rats should show greater-than-normal fear in an out-of-context test. In my doctoral work (Nadel, 1968) I showed exactly this effect, but did not at that time understand what it was telling me. Rats with dorsal hippocampal lesions tested in context B for fear of a CS paired with shock in context A actually showed more fear than did control rats. This finding parallels the Penick and Solomon (1991) result noted above, and is consistent with the report by Good and Honey (1991) showing that hippocampal lesions impaired rats’ ability to learn that a stimulus was reinforced in one context but not in another (see also Lehmann et al., 2005; but see Hall et al., 1996). It is also consistent with the recent findings that hippocampal inactivation impairs the context specificity of latent inhibition (Maren and Holt, 2000), and extinction (Corcoran et al., 2005; Hobin et al., 2006), and that reinstatement of conditioned fear in humans is context specific (LaBar & Phelps, 2005).
Anmerkungen

The source is given on the previous page, but with no indication that the passage here is taken from it more or less verbatim.

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[As such, the “context” representation that supports] conditioned fear after several weeks is a representation based on elements present in the test situation rather than a configural representation of the whole.

Such an explanation mirrors findings pertaining to the ‘pre-exposure’ effect. In this case, when an animal is given fear training without some exposure to the training context prior to the introduction of the unconditioned stimulus, it fails to learn to associate shock with the “context” understood as the configuration of elements (and their spatial relations) in the chamber. This happens, according to Nadel, because exposure to the shock chamber is essential for the animal to acquire a configural representation of the context in the first place – what is termed a ‘cognitive map’ (O’Keefe & Nadel, 1978), or a contextual representation (Nadel & Willner, 1980). According to Nadel, such a finding parallels what happens over time within the realm of consolidation. Initial training (with pre-exposure) leads the animal to associate fear with the configurally-represented context. As such, the behavior depends upon the hippocampus as well as the amygdala. Over time, and as a direct consequence of what has been termed consolidation, the contextual binding weakens, leaving behind only linkages between elements of the chamber and the shock.

These considerations make it much easier to understand the existing literature concerning context and hippocampal lesion effects and why doubts still exist about hippocampal involvement in context learning (e.g., Gewirtz et al., 2000). When “normal” behavior depends upon a configural representation of context, hippocampal lesions will lead to impairment (Nadel, 2008). This should be the case for both acquisition and retention. When a task is used that can be solved with either a configural or an elemental representation of context, hippocampal lesions will not cause an obvious impairment; rather, special testing methods will have to be used to show that performance differs between animals with hippocampal lesions and control animals. The most obvious method would be to shift the test context.

[page 5]

[Instead of assuming that “memory” is either transferred from hippocampus to neocortex, or given independent status within neocortex after a period of requiring hippocampal help in retrieval,] one can best account for the data by assuming that the “context” representation that supports conditioned fear after several weeks is a representation based on elements in the test situation rather than a configural representation of the whole.

[page 6]

This story connects with what has been learned from studying the pre-exposure effect (cf. Fanselow’s work and Rudy’s work). When an animal is given fear training without some exposure to the training context before US introduction, it fails to learn to associate shock with the “context” understood as the configuration of elements (and their spatial relations) in the chamber. This happens because exposure to the shock chamber is essential for the animal to acquire a configural representation of the context in the first place – what we called a cognitive map (O’Keefe and Nadel, 1978), or a contextual representation (Nadel and Willner, 1980).

I believe that this parallels what happens over time in the consolidation domain. Initial training (with pre-exposure) leads the animal to associate fear with the configurally-represented context. As such, the behavior depends upon the hippocampus as well as the amygdala. Over time, and as a direct consequence of what has been called consolidation, the contextual binding weakens, leaving behind only linkages between elements of the chamber and the shock.

These considerations make it much easier to understand the existing literature on hippocampal lesion effects and context and why doubts still exist about hippocampal involvement in context learning (e.g., Gewirtz et al., 2000). When “normal” behavior depends upon a configural representation of context, hippocampal lesions will lead to impairment. This should be the case in both acquisition and retention. When a task is used that can be solved with either a configural or an elemental representation of context, hippocampal lesions will not cause an obvious impairment; rather, special testing methods will have to be used to show that the basis of performance differs between animals with hippocampal lesions and control animals. The most obvious such method would be to shift the test context.

Anmerkungen

Nadel (2008) is mentioned in the text, but it is not clear to the reader at all that the entire page is copied from the source, which is also not listed in the bibliography.

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[Further, adopting conditioned fear paradigms in animals (e.g., Anagnostras et al., 1999, 2001; Fanselow, 1999, 2000), it has been found that; the hippocampus seems to] be necessary for the acquisition of context fear, and for the retrieval of such fear for days (or weeks) following initial training, but not for retrieval 28 days after training; and the acquisition of context fear itself depends upon the animal having had some previous exposure to the context prior to fear training. In the absence of such experience, context fear does not develop. Research using conditioned fear from studies by Rudy’s, as well as Fanselow’s group (Kim and Fanselow, 1992; Anagnostaras et al., 1999, 2001; Fanselow, 1999, 2000), has demonstrated two very important things: (1) the hippocampus seems to be necessary for acquisition of context fear, and for retrieval of such fear for some days (or weeks) after initial training, but not for retrieval 28 days after training; and (2) the acquisition of context fear itself depends upon the animal having had some exposure to the context before fear training starts. Absent such experience, context fear does not develop.
Anmerkungen

The source is not given.

Sichter
(Hindemith) Schumann

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Slotnick and Schacter (2004) further hypothesized that true recognition is associated with greater contextual reactivation than false recognition. Recent memory retrieval-based studies have provided converging evidence for true recognition-related sensory reactivation of the same cortical regions involved in processing stimulus materials during encoding, including reactivation of motor processing regions during memory for motor sequences (Nyberg et al., 2001), reactivation of auditory processing regions during memory for sounds (Nyberg et al., 2000; Wheeler, Petersen & Buckner, 2000) and reactivation of visual processing regions during memory for pictorial stimuli (Wheeler & Buckner, 2004; Wheeler & Buckner, 2003; Vaidya et al., 2002; Wheeler, Petersen, & Buckner, 2000). Slotnick and Schacter tested their hypothesis in the visual system, given its well-known hierarchical functional-anatomic cortical processing architecture. Using abstract shapes in an old-new recognition memory task, they expected to observe greater true as compared to false recognition-related visual cortical activity.

The researchers reported evidence of a functional-anatomic dichotomy between forms of access to late and early visual processing regions: late visual processing regions supported conscious recognition (and were associated with both true and false recognition), whereas early visual processing regions supported implicit memory (and were preferentially associated with true recognition, as opposed to false recognition). Such results provide direct evidence that previously-reported memory-related reactivation in late visual processing [regions (Wheeler & Buckner, 2004; Wheeler & Buckner, 2003; Vaidya et al., 2002; Wheeler et al., 2000) is accessible to conscious recognition, which previously has only been assumed.]


Nyberg, L., Habib, R., McIntosh, A.R., & Tulving, E. (2000). Reactivation of encoding-related brain activity during memory retrieval. Proceedings of the National Academy of Sciences USA, 97, 11120-11124.

Slotnick, S.D. & Schacter, D.L. (2004). A sensory signature that distinguishes true from false memories. Nature Neuroscience, 7, 664-672.

Vaidya, C.J., Zhao, M., Desmond, J.E., & Gabrieli, J.D. (2002). Evidence for cortical encoding specificity in episodic memory: memoryinduced re-activation of picture processing areas. Neuropsychologia 40, 2136-2143.

Wheeler, M.E. & Buckner, R.L. (2003). Functional dissociation among components of remembering: control, perceived oldness, and content. Journal of Neuroscience, 23, 3869–3880.

Wheeler, M.E. & Buckner, R.L. (2004). Functional–anatomic correlates of remembering and knowing. Neuroimage, 21, 1337– 1349.

Wheeler, M.E., Petersen, S.E., & Buckner, R.L. (2000). Memory’s echo: vivid remembering reactivates sensory-specific cortex. Proceedings of the National Academy of Sciences, 97, 11125- 11129.

[Page 664]

Based upon the differential activity found during true as compared to false recognition in the previous two studies11,13, coupled with findings of greater memory for sensory details during true versus false recognition in behavioral studies8–10, we posited that true recognition is associated with greater sensory reactivation than false recognition. Recent studies examining memory retrieval have provided converging evidence for true recognition-related sensory reactivation of the same cortical regions involved in processing stimulus materials during encoding, including reactivation of motor processing regions during memory for motor sequences19, reactivation of

[Page 665]

auditory processing regions during memory for sounds20,21 and reactivation of visual processing regions during memory for pictorial stimuli17,21–23. Capitalizing on these findings, we tested our hypothesis in the visual system, given its well-known hierarchical functional-anatomic cortical processing architecture.

In the present event-related fMRI study, we used abstract shapes in an old-new recognition memory task (Fig. 1; see Methods). According to our sensory reactivation hypothesis, we expected to observe greater true as compared to false recognition-related visual cortical activity. [...]

Here we report evidence of a functional-anatomic dichotomy between forms of access to late and early visual processing regions: late visual processing regions supported conscious recognition (and were associated with both true and false recognition), whereas early visual processing regions supported implicit memory (and were preferentially associated with true recognition, as compared to false recognition). These results provide direct evidence that previously reported memory-related reactivation in late visual processing regions17,21–23 is accessible to conscious recognition, which previously has only been assumed.


8. Schooler, J.W., Gerhard, D. & Loftus, E.F. Qualities of the unreal. J. Exp. Psychol. Learn. Mem. Cogn. 12, 171–181 (1986).

9. Mather, M., Henkel, L.A. & Johnson, M.K. Evaluating characteristics of false memories: remember/know judgments and memory characteristics questionnaire compared. Mem. Cogn. 25, 826–837 (1997).

10. Norman, K.A. & Schacter, D.L. False recognition in younger and older adults: exploring the characteristics of illusory memories. Mem. Cogn. 25, 838–848 (1997).

11. Schacter, D.L. et al. Neuroanatomical correlates of veridical and illusory recognition memory: evidence from positron emission tomography. Neuron 17, 267–274 (1996).

13. Cabeza, R., Rao, S.M., Wagner, A.D., Mayer, A.R. & Schacter, D.L. Can medial temporal lobe regions distinguish true from false? An event-related functional MRI study of veridical and illusory recognition memory. Proc. Natl. Acad. Sci. USA 98, 4805–4810 (2001).

17. Wheeler, M.E. & Buckner, R.L. Functional dissociation among components of remembering: control, perceived oldness, and content. J. Neurosci. 23, 3869–3880 (2003).

19. Nyberg, L. et al. Reactivation of motor brain areas during explicit memory for actions. Neuroimage 14, 521–528 (2001).

20. Nyberg, L., Habib, R., McIntosh, A.R. & Tulving, E. Reactivation of encoding-related brain activity during memory retrieval. Proc. Natl. Acad. Sci. USA 97, 11120–11124 (2000).

21. Wheeler, M.E., Petersen, S.E. & Buckner, R.L. Memory’s echo: vivid remembering reactivates sensory-specific cortex. Proc. Natl. Acad. Sci. USA 97, 11125–11129 (2000).

22. Vaidya, C.J., Zhao, M., Desmond, J.E. & Gabrieli, J.D.E. Evidence for cortical encoding specificity in episodic memory: memory-induced re-activation of picture processing areas. Neuropsychologia 40, 2136–2143 (2002).

23. Wheeler, M.E. & Buckner, R.L. Functional–anatomic correlates of remembering and knowing. Neuroimage 21, 1337–1349 (2004).

Anmerkungen

Taken verbatim with (nearly) all the original references. This is not - as is suggested - a report on the results of Slotnick and Schacter (2004) but a copy of part of the original article, which is not marked as a citation.

Sichter
(Graf Isolan), Hindemith

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[Such results provide direct evidence that previously-reported memory-related reactivation in late visual processing] regions (Wheeler & Buckner, 2004; Wheeler & Buckner, 2003; Vaidya et al., 2002; Wheeler et al., 2000) is accessible to conscious recognition, which previously has only been assumed. Furthermore, this finding purports that the previously reported true-greater-than-false activity assumed to reflect sensory or contextual memory (Schacter et al., 1996; Cabeza et al., 2001) is largely inaccessible to conscious recognition.

Cabeza, R., Rao, S.M., Wagner, A.D., Mayer, A., & Schacter, D.L., (2001). Can medial temporal lobe regions distinguish true from false? An event-related fMRI study of veridical and illusory recognition memory. Proceedings of the National Academy of Sciences USA, 98, 4805-4810.

Slotnick, S.D. & Schacter, D.L. (2004). A sensory signature that distinguishes true from false memories. Nature Neuroscience, 7, 664-672.

Vaidya, C.J., Zhao, M., Desmond, J.E., & Gabrieli, J.D. (2002). Evidence for cortical encoding specificity in episodic memory: memoryinduced re-activation of picture processing areas. Neuropsychologia 40, 2136-2143.

Wheeler, M.E. & Buckner, R.L. (2003). Functional dissociation among components of remembering: control, perceived oldness, and content. Journal of Neuroscience, 23, 3869–3880.

Wheeler, M.E. & Buckner, R.L. (2004). Functional–anatomic correlates of remembering and knowing. Neuroimage, 21, 1337– 1349.

Wheeler, M.E., Petersen, S.E., & Buckner, R.L. (2000). Memory’s echo: vivid remembering reactivates sensory-specific cortex. Proceedings of the National Academy of Sciences, 97, 11125- 11129.

These results provide direct evidence that previously reported memory-related reactivation in late visual processing regions17,21–23 is accessible to conscious recognition, which previously has only been assumed. Furthermore, the present results suggest that the previously reported true-greater-than-false activity assumed to reflect sensory or contextual memory11,13 is largely inaccessible to conscious recognition.

11. Schacter, D.L. et al. Neuroanatomical correlates of veridical and illusory recognition memory: evidence from positron emission tomography. Neuron 17, 267–274 (1996).

13. Cabeza, R., Rao, S.M., Wagner, A.D., Mayer, A.R. & Schacter, D.L. Can medial temporal lobe regions distinguish true from false? An event-related functional MRI study of veridical and illusory recognition memory. Proc. Natl. Acad. Sci. USA 98, 4805–4810 (2001).

17. Wheeler, M.E. & Buckner, R.L. Functional dissociation among components of remembering: control, perceived oldness, and content. J. Neurosci. 23, 3869–3880 (2003).

21. Wheeler, M.E., Petersen, S.E. & Buckner, R.L. Memory’s echo: vivid remembering reactivates sensory-specific cortex. Proc. Natl. Acad. Sci. USA 97, 11125–11129 (2000).

22. Vaidya, C.J., Zhao, M., Desmond, J.E. & Gabrieli, J.D.E. Evidence for cortical encoding specificity in episodic memory: memory-induced re-activation of picture processing areas. Neuropsychologia 40, 2136–2143 (2002).

23. Wheeler, M.E. & Buckner, R.L. Functional–anatomic correlates of remembering and knowing. Neuroimage 21, 1337–1349 (2004).

Anmerkungen

See Jm/Fragment_112_07, where the text begins.

Sichter
(Graf Isolan), Hindemith

[49.] Jm/Fragment 086 01 - Diskussion
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Hans Selye (1956) argued that the stress response, which includes HPA activation, was nonspecific: all stressors, whether physical or psychological, would elicit the same physiological reaction. Others have concluded from the early work investigating the effects of severe physically traumatic experiences on cortisol activity (e.g., electric shock, injury) that only extreme or prolonged stressful conditions trigger cortisol elevations. Some have focused on the specific characteristics of the stressor, hypothesizing that contexts that are novel (Rose, 1980), unpredictable (Mason, 1968), uncontrollable (Henry & Grim, 1990; Sapolsky, 1993), or threatening, with the potential for harm or loss (Blascovich & Tomaka, 1996; Dienstbier, 1989), would be most likely to activate this system. However, even though a range of hypotheses have been put forward, the vast majority has not been empirically investigated, and the evidence, where present, is not conclusive.

Blascovich, J. & Tomaka, J. (1996). The Biopsychosocial Model of Arousal Regulation. Advances in Experimental Social Psychology, 28, 1-46.

Dienstbier, R.A. (1989). Arousal and physiological toughness: Implications for mental and physical health. Psychological Review, 96(1), 84-100.

Henry, J.P. & Grim, C.E. (1990). Psychosocial mechanisms of primary hypertension. Journal of Hypertension 8, 783–793.

Mason, J.W. (1968). A review of psychoendocrine research on the pituitary-adrenal cortical system. Psychosomatic Medicine, 30, 576–607.

Rose, R.M. (1980). Endocrine responses to stressful psychological events. Advances in psychoneuroendocrinology. Psychiatric Clinics of North America, 3, 251–276.

Selye, H. (1956). The Stress of Life. New York: McGraw-Hill.

Hans Selye (1956) argued that the stress response, which includes HPA activation, was nonspecific: All stressors, whether physical or psychological, would elicit the same physiological reaction. Others have concluded from the early work investigating the effects of severe traumatic experiences on cortisol activity (e.g., electric shock, injury) that only extreme or prolonged stressful conditions trigger cortisol elevations. Some have focused on the specific characteristics of the stressor, hypothesizing that contexts that are novel (Rose, 1980), unpredictable (Mason, 1968), uncontrollable (Henry & Grim, 1990; Sapolsky, 1993), or threatening, with the potential for harm or loss (Blascovich & Tomaka, 1996; Dienstbier, 1989), would be most likely to activate this system. Although a number of hypotheses have been offered, many have never been empirically tested, and in other cases, the evidence is not as conclusive as popular wisdom may suggest.

Blascovich, J., & Tomaka, J. (1996). The biopsychosocial model of arousal regulation. Advances in Experimental Social Psychology, 28, 1–51.

Dienstbier, R. A. (1989). Arousal and physiological toughness: Implications for mental and physical health. Psychological Review, 96, 84–100.

Henry, J. P., & Grim, C. E. (1990). Psychosocial mechanisms of primary hypertension. Journal of Hypertension, 8, 783–793.

Mason, J. W. (1968). A review of psychoendocrine research on the pituitary-adrenal cortical system. Psychosomatic Medicine, 30, 576–607.

Rose, R. M. (1980). Endocrine responses to stressful psychological events. Psychiatric Clinics of North America, 3, 251–276.

Sapolsky, R. M. (1993). Endocrinology alfresco: Psychoendocrine studies of wild baboons. Recent Progress in Hormone Research, 48, 437–468.

Selye, H. (1956). The stress of life. New York: McGraw-Hill.

Anmerkungen

Nothing is marked as a citation. Only at the end of the paragraph the author tries to put what can be found in Dickerson and Kemeny (2004) into her own words.

A reference to Sapolsky (1993) is missing in the thesis.

Sichter
(Graf Isolan), Hindemith

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An extensive animal and human literature reports that psychological factors can influence the hypothalamic–pituitary–adrenocortical (HPA) axis, which regulates the release of cortisol (see Chapter 1). Over the past half century, many studies have specifically focused on the effects of psychological stressors on cortisol activation. Despite the extensive magnitude of this research, Dickerson and Kemeny (2004) drew two broad conclusions from this literature as a whole. First, like physical stressors, psychological stressors are indeed capable of activating the HPA axis; a number of studies have reported that laboratory tasks such as public speaking or mental arithmetic can increase cortisol levels (e.g., Kirschbaum, Pirke, & Hellhammer, 1993). Second, the effects of psychological stressors on this physiological system are highly variable. Many studies have failed to find cortisol changes (e.g., Manuck et al., 1991), and recent reviews have highlighted the inconsistent effects of psychological stressors on cortisol activity (e.g., Biondi & Picardi, 1999). The vast heterogeneity in the literature indicates that all types of negative situations may not uniformly trigger cortisol changes (Mason, 1968).

Biondi, M. & Picardi, A. (1999): Psychological stress and neuroendocrine function in humans: the last two decades of research., Psychotherapy and Psychosomatics, 68(3), 114-50.

Dickerson, S. S. & Kemeny, M. E. (2004). Acute stressors and cortisol responses: A theoretical integration and synthesis of laboratory research. Psychological Bulletin, 130(3), 355-391.

Kirschbaum, C., Pirke, K.M., & Hellhammer, D. H. (1993). The "Trier Social Stress Test" - a tool for investigating psychobiology stress responses in a laboratory setting. Neuropsychobiology, 28, 76-81.

Manuck, S.B., Cohen, S., Rabin, B.S., Muldoon, M.F., & Bachen, E.A. (1991). Individual differences in cellular immune responses to stress. Psychological Science, 2, 111-115.

Mason, J.W. (1968). A review of psychoendocrine research on the pituitary-adrenal cortical system. Psychosomatic Medicine, 30, 576–607.

An extensive animal and human literature documents that psychological factors can influence the hypothalamic–pituitary–adrenocortical (HPA) axis, which regulates the release of cortisol, an important hormone associated with psychological, physiological, and physical health functioning. Over the past half century, hundreds of studies have specifically focused on the effects of psychological stressors on cortisol activation. Despite the magnitude of this research enterprise, only two broad conclusions can be drawn from this literature as a whole. First, like physical stressors (e.g., electric shock, prolonged exercise), psychological stressors are indeed capable of activating the HPA axis; a number of studies have reported that laboratory tasks such as public speaking or mental arithmetic can increase cortisol levels (e.g., Kirschbaum, Pirke, & Hellhammer, 1993). Second, the effects of psychological stressors on this physiological system are highly variable. Many studies have failed to find cortisol changes (e.g., Manuck, Cohen, Rabin, & Muldoon, 1991), and recent narrative reviews have highlighted the inconsistent effects of psychological stressors on cortisol activity (e.g., Biondi & Picardi, 1999). The tremendous heterogeneity in the literature suggests that all types of negative situations may not uniformly trigger cortisol changes (Mason, 1968).

Biondi, M., & Picardi, A. (1999). Psychological stress and neuroendocrine function in humans: The last two decades of research. Psychotherapy & Psychosomatics, 68, 114–150.

Kirschbaum, C., Pirke, K. M., & Hellhammer, D. H. (1993). The “Trier Social Stress Test” — A tool for investigating psychobiological stress responses in a laboratory setting. Neuropsychobiology, 28, 76–81.

*Manuck, S. B., Cohen, S., Rabin, B. S., & Muldoon, M. F. (1991). Individual differences in cellular immune response to stress. Psychological Science, 2, 111-115.

Mason, J. W. (1968). A review of psychoendocrine research on the pituitary-adrenal cortical system. Psychosomatic Medicine, 30, 576–607.

Anmerkungen

The extent of verbatim appropriation has not been marked.

Sichter
(Graf Isolan), Hindemith

[51.] Jm/Fragment 036 01 - Diskussion
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[Given that MRs are largely occupied] during rest and GRs become activated during stress, most researchers have concluded that activation of GRs, rather than MRs, are responsible for stress-related brain and behavioral changes (see Roozendaal, 1999).

Thus stress sets in motion a number of physiological responses, including sympathetic and HPA activation and the release of stress hormones. These hormones exert their action in the brain by activating corticosteroid receptors. The distribution of these receptors in structures involved in memory, particularly the hippocampus (which has the largest concentration of receptors) is an important link in understanding the connection between glucocorticoids and cognition.

1.3.3 Stress & Memory: Animal Studies

The animal literature on stress and cognition is vast, providing robust evidence that stress or administered corticosteroids affect both associative learning and spatial memory. Stress manipulations include social stress (dominance struggle), physical restraint, shock, and certain stressful tasks, while corticosteroid administration involves either injection, implanted hormone “beads,” or intracerebral administration. Investigators have examined the modulatory effects of corticosteroids following adrenalectomy (or other lesion procedure), and the direct effects of administered hormones or stress in healthy animals. Researchers have also experimented with the timing and dose of the manipulation. Together, these studies provide a complex picture, but suggest a facilitative effect of moderate doses of corticosteroids (or moderate stress) on encoding and consolidation, and possibly an adverse effect on retrieval. Given current limitations, only human studies will be discussed.


Roozendaal, B. (1999). Glucocorticoids and the regulation of memory consolidation. Psychoneuroendocrinology, 25, 213-238.

[Page 13]

Because MRs are largely occupied during rest and GRs become activated during stress, most researchers have concluded that activation of GRs, rather

[Page 14]

than MRs, are responsible for stress-related brain and behavioral changes (see Roozendaal, 1999).

[Page 15]

Thus stress sets in motion a number of physiological responses, including sympathetic and HPA activation and the release of stress hormones. These hormones exert their action in the brain by activating corticosteroid receptors. The distribution of these receptors in structures involved in memory, particularly the hippocampus (which has the largest concentration of receptors) is an important link in understanding the connection between glucocorticoids and cognition.

[Page 28]

4. Stress & Memory: Animal Studies

Introduction

The animal literature on stress and cognition is vast, providing robust evidence that stress or admininstered [sic] corticosteroids affect both associative learning and spatial memory. Stress manipulations include social stress (dominance struggle), physical restraint, shock, and certain stressful tasks, while corticosteroid administration involves either injection, implanted hormone “beads,” or intracerebral administration. Investigators have examined the modulatory effects of corticosteroids following adrenalectomy (or other lesion procedure), and the direct effects of administered hormones or stress in healthy animals. Researchers have also experimented with the timing and dose of the manipulation. Together, these studies provide a complex picture, but suggest a facilitative effect of moderate doses of corticosteroids (or moderate stress) on encoding and consolidation, and possibly an adverse effect on retrieval.


Roozendaal, B. (2000). Glucocorticoids and the regulation of memory consolidation. Psychoneuroendocrinology, 25, 213-238.

Anmerkungen

A collage of original pieces from the PhD-thesis of Beckner (2004). The source is never named though the pieces are taken verbatim, with even the emphasized words being mostly the same.

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(Graf Isolan), Hindemith

[52.] Jm/Fragment 023 01 - Diskussion
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[Related to context-dependent traumatic memory, and importantly in terms of possible therapeutic research directions within the realm of reconsolidation, central aspects of] emotional experiences are often remembered at the expense of incidental background details (Payne, Nadel, Britton, & Jacobs, 2004; Reisberg & Heuer, 2004). A real-world example of this trade-off is the weapon-focus effect, wherein victims vividly remember an assailant’s weapon but have little memory for other integral aspects of the scene (Stanny & Johnson, 2000; Loftus, Loftus & Messo, 1987). This divergence in memory for central and peripheral aspects of emotional events reflects, at least in part, differential encoding of these two components of the scene. At present, it is unclear how the components of emotional episodic memories are processed and stored and whether they change over time or remain the same. Emotional scenes could be stored as intact units, undergoing some forgetting over time but retaining the same relative vividness for central and peripheral components. Alternatively, the components of the scene could undergo differential processing and storage, perhaps with a selective emphasis on what is most salient and worthy of remembering. Rather, central, emotional information is often remem­bered at the expense of background details (Payne, Nadel, Britton, & Jacobs, 2004; Reisberg & Heuer, 2004). A real-world example of this trade-off is the weapon-focus effect, wherein victims vividly remember an assailant’s weapon but have little memory for other important aspects of the scene (Stanny & Johnson, 2000). This divergence in memory for central and peripheral aspects of emotional events reflects, at least in part, differential encoding of these two components of the scene. But it is also possible that these elements undergo qualitatively different processing subsequent to encoding.

At present, it is unclear how the components of emotional memories are processed and stored, whether they change over time or remain the same, and whether periods of sleep affect their consolidation differently than periods spent awake. Emo­tional scenes could be stored as intact units, undergoing some forgetting over time but retaining the same relative vividness for central and peripheral components. Alternatively, the compo­nents of the scene could undergo differential processing and storage, perhaps with a selective emphasis on what is most sa­lient and worthy of remembering.

Anmerkungen

The source is not given here, only further down in the paragraph without providing a reference for the here documented passage.

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[Many studies have found an impairing effect of cortisol on word or narrative recall by using both] psychosocial stress (Jelicic [sic], Geraerts, Merckelbach, & Guerrieri, 2004; Wolf et al., 2001) and glucocorticoid administration (Kirschbaum et al., 1996; Tops et al., 2003), although it is pertinent to note that these studies applied the stressor or glucocorticoid prior to stimulus presentation and tested recall within an hour of the manipulation, thereby elevating cortisol during encoding, consolidation, and retrieval. The detrimental effects of stress on memory in these studies may thus be due to impaired retrieval (Beckner et al., 2006).

Beckner, V.E., Tucker, D.M., Delville, Y., & Mohr, D.C. (2006). Stress facilitates consolidation of verbal memory for a film but does not affect retrieval. Behavioural Neuroscience, 120, 518-527.

Jelici, M., Geraerts, E., Merckelbach, H., & Guerrieri, R. (2004). Acute stress enhances memory for emotional words, but impairs memory for neutral words. International Journal of Neuroscience, 114, 1343–1351.

Kirschbaum, C., Wolf, O.T., May, M., Wippich, W., & Hellhammer, D.H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475-1483.

Tops, M., van der Pompe, G., Baas, D., Mulder, L.J., Den Boer, J.A., Meijman, T.F., Korf, J. (2003). Acute cortisol effects on immediate free recall and recognition of nouns depend on stimulus valence. Psychophysiology, 40, 167-173.

Wolf, O.T., Convit, A., McHugh, P.F., Kandil, E., Thorn, E.L., De Santi, S., McEwen, B.S., & de Leon, M.J. (2001a). Cortisol differentially affects memory in young and elderly men. Behavioural Neuroscience, 105, 1002-1011.

Wolf, O.T., Schommer, N.C., Hellhammer, D.H., McEwen, B.S., & Kirschbaum, C. (2001b). The relationship between stress induced cortisol levels and memory differs between men and women. Psychoneuroendocrinology, 26, 711-720.

Many studies have found an impairing effect of cortisol on word or narrative recall by using both psychosocial stress (Jelici, Geraerts, Merckelbach, & Guerrieri, 2004; Wolf, Schommer, et al., 2001) and glucocorticoid administration (Kirschbaum et al., 1996; Tops et al., 2003), although these studies applied the stressor or glucocorticoid prior to stimulus presentation and tested recall within an hour of the manipulation, thereby elevating cortisol during encoding, consolidation, and retrieval. The detrimental effects of stress on memory in these studies may be due to impaired retrieval.

Jelici, M., Geraerts, E., Merckelbach, H., & Guerrieri, R. (2004). Acute stress enhances memory for emotional words, but impairs memory for neutral words. International Journal of Neuroscience, 114, 1343-1351.

Kirschbaum, C., Wolf, O. T., May, M., Wippich, W., & Hellhammer, D. H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475-1483.

Tops, M., van der Pompe, G., Baas, D., Mulder, L. J., Den Boer, J. A., Meijman, T. F., et al. (2003). Acute cortisol effects on immediate free recall and recognition of nouns depend on stimulus valence. Psychophysiology, 40, 167-173.

Wolf, O. T., Schommer, N. C., Hellhammer, D. H., McEwen, B. S., & Kirschbaum, C. (2001). The relationship between stress induced cortisol levels and memory differs between men and women. Psychoneuroendocrinology, 26, 711-720.

Anmerkungen

Although the source is given, it is not made clear how detailed the takeover has been. No part of the text is marked as a citation.

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(Graf Isolan), Hindemith

[54.] Jm/Fragment 040 20 - Diskussion
Bearbeitet: 17. January 2014, 20:55 Hindemith
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Results provided support for the facilitative effect of stress and endogenous cortisol on the consolidation of new information, providing the first evidence that stress enhances the consolidation of verbal information. Indeed, this evidence for a facilitative effect of stress on the consolidation of verbal memory stood in contrast with much of the literature. Many studies have found an impairing effect of cortisol on word or narrative recall by using both [psychosocial stress (Jelicic [sic], Geraerts, Merckelbach, & Guerrieri, 2004; Wolf et al., 2001) and glucocorticoid administration (Kirschbaum et al., 1996; Tops et al., 2003), although it is pertinent to note that these studies applied the stressor or glucocorticoid prior to stimulus presentation and tested recall within an hour of the manipulation, thereby elevating cortisol during encoding, consolidation, and retrieval.]

Jelici, M., Geraerts, E., Merckelbach, H., & Guerrieri, R. (2004). Acute stress enhances memory for emotional words, but impairs memory for neutral words. International Journal of Neuroscience, 114, 1343–1351.

Kirschbaum, C., Wolf, O.T., May, M., Wippich, W., & Hellhammer, D.H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475-1483.

Tops, M., van der Pompe, G., Baas, D., Mulder, L.J., Den Boer, J.A., Meijman, T.F., Korf, J. (2003). Acute cortisol effects on immediate free recall and recognition of nouns depend on stimulus valence. Psychophysiology, 40, 167-173.

Wolf, O.T., Convit, A., McHugh, P.F., Kandil, E., Thorn, E.L., De Santi, S., McEwen, B.S., & de Leon, M.J. (2001a). Cortisol differentially affects memory in young and elderly men. Behavioural Neuroscience, 105, 1002-1011.

Wolf, O.T., Schommer, N.C., Hellhammer, D.H., McEwen, B.S., & Kirschbaum, C. (2001b). The relationship between stress induced cortisol levels and memory differs between men and women. Psychoneuroendocrinology, 26, 711-720.

The results provide support for the facilitative effect of stress and endogenous cortisol on the consolidation of new information — and provide the first evidence of this for verbal information by using a stress manipulation. [...]

Indeed, our evidence for a facilitative effect of stress on the consolidation of verbal memory is a new finding and in contrast to much of the literature. Many studies have found an impairing effect of cortisol on word or narrative recall by using both psychosocial stress (Jelici, Geraerts, Merckelbach, & Guerrieri, 2004; Wolf, Schommer, et al., 2001) and glucocorticoid administration (Kirschbaum et al., 1996; Tops et al., 2003), although these studies applied the stressor or glucocorticoid prior to stimulus presentation and tested recall within an hour of the manipulation, thereby elevating cortisol during encoding, consolidation, and retrieval.


Jelici, M., Geraerts, E., Merckelbach, H., & Guerrieri, R. (2004). Acute stress enhances memory for emotional words, but impairs memory for neutral words. International Journal of Neuroscience, 114, 1343–1351.

Kirschbaum, C., Wolf, O. T., May, M., Wippich, W., & Hellhammer, D. H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475–1483.

Tops, M., van der Pompe, G., Baas, D., Mulder, L. J., Den Boer, J. A., Meijman, T. F., et al. (2003). Acute cortisol effects on immediate free recall and recognition of nouns depend on stimulus valence. Psychophysiology, 40, 167–173.

Wolf, O. T., Schommer, N. C., Hellhammer, D. H., McEwen, B. S., & Kirschbaum, C. (2001). The relationship between stress induced cortisol levels and memory differs between men and women. Psychoneuroendocrinology, 26, 711–720.

Anmerkungen

At the end of the paragraph on the following page the source is named (cp. Jm/Fragment_041_01). Otherwise nothing is marked as a citation.

Sichter
(Graf Isolan), Hindemith

[55.] Jm/Fragment 037 02 - Diskussion
Bearbeitet: 17. January 2014, 20:49 Hindemith
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Although research clearly demonstrates that chronically elevated cortisol (from disease, corticosteroid treatment, or aging) is associated with impairments in declarative memory (Lupien et al., 2004, 1998; Martignoni et al., 1992), evidence for acute effects is mixed. Early experimental studies using stress induction or single-dose glucocorticoid administration showed an impairing effect of acutely elevated cortisol on verbal declarative memory (Kirschbaum et al., 1996; Newcomer et al., 1994; Wolf et al., 2001; Wolkowitz et al., 1990). However, recent studies investigating acute effects of cortisol on word recall either failed to replicate these findings by using cortisol administration (Hsu et al., 2003) or psychosocial stress (Wolf et al., 2001) or obtained opposite findings (Domes et al., 2002).

One explanation for these discrepancies, according to Beckner and colleagues (2006), may be due to differences in dose levels of glucocorticoids. Both animal and human data suggest an inverted U-shaped function between glucocorticoids and memory (see Lupien & McEwen, 1997, for a review).


Beckner, V.E., Tucker, D.M., Delville, Y., & Mohr, D.C. (2006). Stress facilitates consolidation of verbal memory for a film but does not affect retrieval. Behavioural Neuroscience, 120, 518-527.

Domes, G., Heinrichs, M., Reichwald, U., & Hautzinger, M. (2002). Hypothalamic–pituitary-adrenal axis reactivity to psychological stress and memory in middle-aged women: high responders exhibit enhanced declarative memory performance. Psychoneuroendocrinology, 27, 843.

Hsu, F.C., Garside, M.J., Massey, A.E., & McAllister-Williams, R.H. (2003). Effects of a single dose of cortisol on the neural correlates of episodic memory and error processing in healthy volunteers. Psychopharmacology , 167, 431-442.

Kirschbaum, C., Wolf, O.T., May, M., Wippich, W., & Hellhammer, D.H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475-1483.

Lupien, S.J., de Leon, M., de Santi, S., Convit, A., Tarshish, C., Nair, N.P., Thakur, M., McEwen, B.S., Hauger, R.L., & Meaney, M.J. (1998). Cortisol levels during human aging predict hippocampal atrophy and memory deficits. Nature Neuroscience, 1, 3–4.

Lupien, S.J., DeLeon, M., DeSanti, S., Convit, A., Tarshish, C., Nair, N.P.V., McEwen, B.S., Hauger, R.L., & Meaney, M.J. (1998). Longitudinal increase in cortisol during human aging predicts hippocampal atrophy and memory deficits. Nature Neuroscience, 1, 69-73.

Martignoni, E., Costa, A., & Sinforiani, E. (1992). The brain as a target for adrenocortical steroids: cognitive implications. Psychoneuroendocrinology, 17, 343-354.

Newcomer, J.W., Craft, S., Hershey, T., Askins, K., & Bardgett, M.E. (1994). Glucocorticoidinduced impairment in declarative memory performance in adult humans. Journal of Neuroscience, 14, 2047–2053.

Wolf, O.T., Convit, A., McHugh, P.F., Kandil, E., Thorn, E.L., De Santi, S., McEwen, B.S., & de Leon, M.J. (2001a). Cortisol differentially affects memory in young and elderly men. Behavioural Neuroscience, 105, 1002-1011.

Wolf, O.T., Schommer, N.C., Hellhammer, D.H., McEwen, B.S., & Kirschbaum, C. (2001b). The relationship between stress induced cortisol levels and memory differs between men and women. Psychoneuroendocrinology, 26, 711-720.

Although research clearly demonstrates that chronically elevated cortisol (from disease, corticosteroid treatment, or aging) is associated with impairments in declarative memory (Lupien et al., 1998; Martignoni et al., 1992; Starkman & Schteingart, 1981; Wolkowitz, Lupien, Bigler, Levin, & Canick, 2004), evidence for acute effects is mixed. Early experimental studies using a stress induction or single-dose glucocorticoid administration showed an impairing effect of acutely elevated cortisol on verbal declarative memory (Kirschbaum, Wolf, May, Wippich, & Hellhammer, 1996; Newcomer, Craft, Hershey, Askins, & Bardgett, 1994; Wolf, Schommer, Hellhammer, McEwen, & Kirschbaum, 2001; Wolkowitz et al., 1990). However, recent studies looking at acute effects of cortisol on word recall either failed to replicate these findings by using cortisol administration (Hsu, Garside, Massey, & McAllister-Williams, 2003) or psychosocial stress (Wolf, Convit, et al., 2001) or obtained opposite findings (Domes, Heinrichs, Reichwald, & Hautzinger, 2002). One explanation for these discrepancies may be due to differences in dose: Animal and human data suggest an inverted U-shaped function between glucocorticoids and memory (see Lupien & McEwen, 1997, for a review).

Domes, G., Heinrichs, M., Reichwald, U., & Hautzinger, M. (2002). Hypothalamic–pituitary-adrenal axis reactivity to psychological stress and memory in middle-aged women: High responders exhibit enhanced declarative memory performance. Psychoneuroendocrinology, 27, 843– 853.

Hsu, F. C., Garside, M. J., Massey, A. E., & McAllister-Williams, R. H. (2003). Effects of a single dose of cortisol on the neural correlates of episodic memory and error processing in healthy volunteers. Psychopharmacology, 167, 431–442.

Kirschbaum, C., Wolf, O. T., May, M., Wippich, W., & Hellhammer, D. H. (1996). Stress- and treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences, 58, 1475–1483.

Lupien, S. J., de Leon, M., de Santi, S., Convit, A., Tarshish, C., Nair, N. P., et al. (1998). Cortisol levels during human aging predict hippocampal atrophy and memory deficits. Nature Neuroscience, 1, 69–73.

Lupien, S. J., & McEwen, B. S. (1997). The acute effects of corticosteroids on cognition: Integration of animal and human model studies. Brain Research Reviews, 24, 1–27.

Martignoni, E., Costa, A., Sinforiani, E., Liuzzi, A., Chiodini, P., Mauri, M., et al. (1992). The brain as a target for adrenocortical steroids: Cognitive implications. Psychoneuroendocrinology, 17, 343–354.

Newcomer, J. W., Craft, S., Hershey, T., Askins, K., & Bardgett, M. E. (1994). Glucocorticoid-induced impairment in declarative memory performance in adult humans. Journal of Neuroscience, 14, 2047–2053.

Starkman, M. N., & Schteingart, D. E. (1981). Neuropsychiatric manifestations of patients with Cushing’s syndrome. Relationship to cortisol and adrenocorticotropic hormone levels. Archives of Internal Medicine, 141, 215–219.

Wolf, O. T., Convit, A., McHugh, P. F., Kandil, E., Thorn, E. L., De Santi, S., et al. (2001). Cortisol differentially affects memory in young and elderly men. Behavioral Neuroscience, 115, 1002–1011.

Wolf, O. T., Schommer, N. C., Hellhammer, D. H., McEwen, B. S., & Kirschbaum, C. (2001). The relationship between stress induced cortisol levels and memory differs between men and women. Psychoneuroendocrinology, 26, 711–720.

Wolkowitz, O. M., Reus, V. I., Weingartner, H., Thompson, K., Breier, A., Doran, A., et al. (1990). Cognitive effects of corticosteroids. American Journal of Psychiatry, 147, 1297–1303.

Anmerkungen

There is no entry for Wolkowitz et al. (1990) in the list of references in Jm.

Nothing has been marked as a citation. The source of this paragraph is mentioned in passing in the second paragraph.

Sichter
(Graf Isolan), Hindemith

[56.] Jm/Fragment 097 17 - Diskussion
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Salivette swabs are available with a citric acid infusion to stimulate saliva flow, but the citric acid is liable to affect pH levels of samples, and is thus to be avoided. Since the untreated pure cotton swabs, employed herein, supplied with standard Salivette tubes usually collect a sound sample of 1½ - 2 ml of saliva after between 60-80s of chewing, obtaining a sufficient sample is usually unproblematic (Kirschbaum & Hellhammer, 2000). SalivetteTM swabs are available with a citric acid infusion to stimulate saliva flow, but the citric acid is liable to affect pH levels of samples, and is thus to be avoided. Since the untreated pure cotton swabs supplied with standard SalivetteTM tubes usually collect a sound sample of 1½ - 2 ml of saliva after between 60-80s of chewing, obtaining a sufficient sample is usually unproblematic.
Anmerkungen

The source is not referenced.

Sichter
(Hindemith) Schumann

[57.] Jm/Fragment 020 01 - Diskussion
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[Indeed according to the Encoding Specificity Principle (Tulving, 1974; Tulving & Thomson, 1973), memory for attended aspects of an encoded event (i.e., item memory) is facilitated] when features of the encoding context are reinstated at test, thereby indicating that item and context features are bound together in memory traces (Smith, 1979). At a basic level, the Encoding Specificity Principle suggests that episodic memory will be improved when contextual cues are provided. The cues will reinstate encoding conditions, and this should increase access to all encoded information, including incidentally processed contextual details. Memory for attended aspects of an encoded event (item memory) is facilitated when features of the encoding context are reinstated at test, indicating that item and context features are bound together in memory traces (Smith, 1979).

[page 2]

At a basic level, the encoding-specificity principle suggests that source memory will be improved when contextual cues are provided. The cues will reinstate encoding conditions, and this should increase access to all encoded information, including incidentally processed contextual details.

Anmerkungen

There is no reference to the source.

Sichter
(Hindemith) Schumann

[58.] Jm/Fragment 091 17 - Diskussion
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2.4.2.3 The Rosenberg Self-Esteem Scale

The Rosenberg Self-Esteem Scale (RSE; Rosenberg, 1965, see Appendix 7) was devised in an attempt to achieve a unidimensional measure of global self-esteem. [...] The scale was originally designed as a Guttman scale, in that the RSE items were to represent a continuum of self-worth statements ranging from statements that are endorsed even by individuals with low self-esteem to statements that are [endorsed only by persons with high self-esteem.]

The Rosenberg Self-Esteem Scale

The Rosenberg Self-Esteem Scale (RSE; Rosenberg 1965) is an attempt to achieve a unidimensional measure of global self-esteem. It was designed to be a Gutman scale, which means that the RSE items were to represent a continuum of self-worth statements ranging from statements that are endorsed even by individuals with low self-esteem to statements that are endorsed only by persons with high self-esteem.

Anmerkungen

A reference to the source is missing.

Sichter
(Hindemith) Schumann

[59.] Jm/Fragment 093 01 - Diskussion
Bearbeitet: 17. January 2014, 20:39 Hindemith
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2.4.2.5 The General Health Questionnaire (GHQ)

The General Health Questionnaire (GHQ; Goldberg, 1978, see Appendix 9) is the most common assessment of mental well-being. Developed as a screening tool to detect those likely to have or be at risk of developing psychiatric disorders, it is a measure of the common mental health problems/domains of depression, anxiety, somatic symptoms and social withdrawal. Available in a variety of versions using 12, 28, 30 or 60 items, the 28-item version is used most widely. Examples of some of the items in use include ‘Have you found everything getting on top of you?’; ‘Have you been getting scared or panicky for no good reason?’ and ‘Have you been getting edgy and bad tempered?’. Each item is accompanied by four possible responses, typically being ‘not at all’, ‘no more than usual’, ‘rather more than usual’ and ‘much more than usual’, scoring from 0 to 3, respectively. The total possible score on the GHQ 28 ranges from 0 to 84. Reliability coefficients have ranged from 0.78 to 0.95 in various studies.

Possibly, the most common assessment of mental well-being is the GHQ. Developed as a screening tool to detect those likely to have or be at risk of developing psychiatric disorders, it is a measure of the common mental health problems/domains of depression, anxiety, somatic symptoms and social withdrawal. Available in a variety of versions using 12, 28, 30 or 60 items, the 28-item version is used most widely. [...]

[...]

Examples of some of the items in use include ‘Have you found everything getting on top of you?’; ‘Have you been getting scared or panicky for no good reason?’ and ‘Have you been getting edgy and bad tempered?’. Each item is accompanied by four possible responses, typically being ‘not at all’, ‘no more than usual’, ‘rather more than usual’ and ‘much more than usual’, scoring from 0 to 3, respectively. The total possible score on the GHQ 28 ranges from 0 to 84 and allows for means and distributions to be calculated, both for the global total, as well as for the four sub-scales. [...]

[...]

Reliability coefficients have ranged from 0.78 to 0.95 in various studies.

Anmerkungen

The content of this paragraph may be common knowledge, but the presentation is taken from the source without attribution.

Sichter
(Hindemith) Schumann

[60.] Jm/Fragment 331 14 - Diskussion
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In support of such a finding, previous studies have observed enhanced consolidation of emotionally arousing material when compared with neutral material following cortisol or stress treatment (Buchanan & Lovallo, 2001; Cahill et al., 2003). [...] Previous studies (e.g., Buchanan & Lovallo, 2001; Kuhlmann et al., 2005) have further suggested that the effects of cortisol are similar for positive as well as negative material, which suggests that emotional arousal rather than valence is the critical aspect of the observed interactions. These observations are in accord with neuroimaging studies showing that the activity of the amygdala is associated with memory formation of arousing stimuli (Cahill et al., 1996; Canli et al., 2000), apparently independent of stimuli valence (Hamann et al., 1999; Kensinger & [Corkin, 2004).]

Buchanan, T.W. & Lovallo, W.R. (2001). Enhanced memory for emotional material following stress-level cortisol treatment in humans. Psychoneuroendocrinology, 26, 307–317.

Cahill L, Gorski L, & Le K (2003). Enhanced human memory consolidation with post-learning stress: interaction with the degree of arousal at encoding. Learning and Memory, 10, 270–274.

Kuhlmann, S., Kirschbaum, C., & Wolf, O.T. (2005a). Effects of oral cortisol treatment in healthy young women on memory retrieval of negative and neutral words. Neurobiology of Learning and Memory, 83, 158–162

Kuhlmann, S., Piel, M., & Wolf, O.T. (2005b). Impaired memory retrieval after psychosocial stress in healthy young men. Journal of Neuroscience, 25, 2977–2982.

[Two previous studies have observed enhanced consolidation] of emotionally arousing material when compared with neutral material after cortisol or stress treatment (Buchanan and Lovallo, 2001; Cahill et al., 2003). [...] In our current study, as well as in previous studies (Buchanan and Lovallo, 2001; Kuhlmann et al., 2005), the effects of cortisol were similar for positive as well as negative material, which suggests that emotional arousal rather than valence is the crucial aspect of the observed interactions. These observations are in accord with neuroimaging studies showing that the activity of the amygdala is associated with memory formation of arousing stimuli (Cahill et al., 1996; Canli et al., 2000), apparently independent of stimuli valence (Hamann et al., 1999; Kensinger and Corkin, 2004).

Buchanan TW, Lovallo WR (2001) Enhanced memory for emotional material following stress-level cortisol treatment in humans. Psychoneuroendocrinology 26:307–317.

Cahill L, Gorski L, Le K (2003) Enhanced human memory consolidation with post-learning stress: interaction with the degree of arousal at encoding. Learn Mem 10:270 –274.

Canli T, Zhao Z, Brewer J, Gabrieli JD, Cahill L (2000) Event-related activation in the human amygdala associates with later memory for individual emotional experience. J Neurosci 20:RC99(1–5).

Hamann SB, Ely TD, Grafton ST, Kilts CD (1999) Amygdala activity related to enhanced memory for pleasant and aversive stimuli. Nat Neurosci 2:289 –293.

Kensinger EA, Corkin S (2004) Two routes to emotional memory: distinct neural processes for valence and arousal. Proc Natl Acad Sci USA 101:3310 –3315.

Kuhlmann S, Kirschbaum C, Wolf OT (2005) Effects of oral cortisol treatment in healthy young women on memory retrieval of negative and neutral words. Neurobiol Learn Mem 83:158 –162.

Anmerkungen

The references for Canli et al. (2000), Hamann et al. (1999) and Kensinger & Corkin (2004) are all missing from Jm.

Nothing has been marked as a citation. The original source is only mentioned in passing - if at all: "Kuhlmann et al., 2005" cannot be found in the list of references. The reader needs to guess if this means "Kuhlmann, S., Kirschbaum, C., & Wolf, O.T. (2005a)" or "Kuhlmann, S., Piel, M., & Wolf, O.T. (2005b)".

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(Graf Isolan) Agrippina1

[61.] Jm/Fragment 043 01 - Diskussion
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Thus far we have herein outlined a plethora of research which has revealed that secretion of GCs due to HPA axis stimulation may modulate memory functioning. However, the precise direction of stress-induced GC effects on memory performance is far from clear. Animal studies, for example, have shown that GCs can have facilitating (e.g., on aversive conditioning), but also impairing effects on memory. Similarly, studies relying on human participants have reported that acute GC administration may enhance or disrupt memory, yet the precise conditions under which these effects occur are ill-understood. Recently, Joëls and colleagues (2006) argued that stress will enhance memory only when the memory acquisition phase and stressor share the same spatiotemporal context (i.e., context-congruency). Smeets and colleagues (2007) tested this hypothesis by examining whether context congruent stress enhances declarative memory performance, as would be predicted by the encoding specificity principle. Participants were assigned to a personality stress group, a memory stress group, or a no-stress control group. While being exposed to the acute stressor or a control task, participants encoded personality and memory-related words and were tested for free recall 24 hours later. Relative to controls, psychosocial stress significantly enhanced recall of contextually-congruent words, but only for personality words. This suggests that acute stress may strengthen the consolidation of memory material when the stressor matches the to-beremembered information in place and time. Recently, Jols et al. [Joëls, M., Pu, Z., Wiegert, O., Oitzl, M.S., Krugers, H.J., 2006. Learning under stress: how does it work? Trends in Cognitive Sciences, 10, 152–158] argued that stress will enhance memory only when the memory acquisition phase and stressor share the same spatiotemporal context (i.e., context-congruency). The current study tested this hypothesis by looking at whether context-congruent stress enhances declarative memory performance. Undergraduates were assigned to a personality stress group (n = 16), a memory stress group (n = 18), or a no-stress control group (n = 18). While being exposed to the acute stressor or a control task, participants encoded personality- and memory-related words and were tested for free recall 24 h later. Relative to controls, stress significantly enhanced recall of context-congruent words, but only for personality words. This suggests that acute stress may strengthen the consolidation of memory material when the stressor matches the to-be-remembered information in place and time.

[...] A plethora of research has revealed that secretion of glucocorticoids (GCs) due to HPA axis stimulation may modulate memory functioning (e.g., de Kloet et al., 1999; McGaugh, 2000; Roozendaal, 2000). However, the precise direction of stress-induced GC effects on memory performance is far from clear. Animal studies, for example, have shown that GCs can have facilitating (e.g., on aversive conditioning), but also impairing effects on memory (e.g., de Kloet et al., 1999; Lupien and McEwen, 1997; McGaugh and Roozendaal, 2002). Similarly, studies relying on human participants have reported that acute GC administration may enhance or disrupt memory, yet the precise conditions under which these effects occur are ill-understood (for reviews, see Het et al., 2005; Lupien et al., 2005; Lupien and Lepage, 2001; Wolf, 2003).

Anmerkungen

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(Hindemith) Singulus

[62.] Jm/Fragment 289 01 - Diskussion
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Presently there is a paucity of human studies concerned with the effects of cortisol on the reconsolidation process. Tollenaar and colleagues (2008a) recently examined the effects of elevated stress hormones on postretrieval processes in humans. In line with animal studies, a postretrieval decline in memory performance was observed when memories were reactivated during stress (i.e., 5 weeks after encoding). More recently Tollenaar and colleagues (2009) examined both the immediate and prolonged effects of a single administered dose of cortisol or propranolol on memory retrieval in healthy young men, with a one week interval between acquisition and retrieval. Memory retrieval for both neutral and emotional information was impaired by a single dose of cortisol compared to placebo. The cortisol-induced memory impairment remained, even following the one week interval. Conversely, no immediate or prolonged effects of propranolol on memory retrieval were found, despite significant reductions in sympathetic arousal. Such a finding lends support to the hypothesis that cortisol is capable of attenuating emotional memory recall over longer time spans and may therefore be more beneficial in terms of augmenting the treatment of disorders such as PTSD and phobias using beta-blockers such a propranolol.

The effect of blocking adrenergic activity during memory reactivation has recently been studied in humans (e.g., Brunet et al., 2008; Miller et al., 2004). Miller and colleagues reported that fear conditioning was reduced when a conditioned cue was reactivated and followed by noradrenaline beta-blockade. Furthermore, Brunet and colleagues found that postretrieval propranolol reduced psycho-physiological responding to mental imagery of a past traumatic event in PTSD.

[page 50]

The present investigation was therefore undertaken to examine the immediate and prolonged effects of a single administered dose of cortisol or propranolol on memory retrieval in a double-blind placebo controlled design. Eightyfive healthy male participants were asked to retrieve previously learned emotional and neutral information after ingestion of 35 mg cortisol, 80 mg propranolol or placebo. After a washout period of one week, recall was again tested. Memory retrieval of neutral and emotional information was impaired by a single dose of cortisol compared to placebo. The memory impairment due to cortisol remained, even after a washout period of 1 week. No immediate or prolonged effects of propranolol on memory retrieval were found, despite significant reductions in sympathetic arousal. These results lend support to the hypothesis that cortisol is able to attenuate (emotional) memory recall in men over longer time spans and may therefore augment the treatment of disorders like post-traumatic stress disorder and phobias, but do not clarify the mechanism(s) through which propranolol exerts its therapeutic effects.

[page 52]

Human studies on reconsolidation and the effects of cortisol and NA on this process are scarce. In a previously reported study, we examined the effects of elevated stress hormones on post-retrieval processes in humans (Tollenaar et al., 2008b / Chapter 3). In line with animal studies (Maroun & Akirav, 2007), a post-retrieval decline in memory performance was observed when memories were reactivated during stress (5 weeks after encoding). [...] The effect of blocking adrenergic activity during memory reactivation has recently been studied in humans by Miller et al. (2004) and Brunet et al. (2008). Miller and colleagues reported that fear conditioning was reduced when a conditioned cue was reactivated and followed by NA beta-blockade. In addition, Brunet and colleagues found that post-retrieval propranolol reduced psycho-physiological responding to mental imagery of a past traumatic event in post-traumatic stress disorder (PTSD).

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Note that according to the list of references "Tollenaar and colleagues (2009)" refers to a different study.

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[63.] Jm/Fragment 004 10 - Diskussion
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Lee and colleagues (2005) found that infusions of Zif268 antisense oligodeoxynucleotides into the basolateral amygdala of rats, prior to the reactivation of a well-learned memory for a conditioned stimulus (CS)-cocaine association, abolished the acquired conditioned reinforcing properties of the drug-associated stimulus and thus its impact on the learning of a new cocaine-seeking response. Furthermore, it was shown that reconsolidation of CS-fear memories also requires Zif268 in the amygdala. These results demonstrate that appetitive CS-drug memories undergo reconsolidation in a manner similar to aversive memories and that this amygdala-dependent reconsolidation can be disrupted to reduce the impact of drug cues on drug seeking.

Lee, J.L., Di Ciano, P., Thomas, K.L., & Everitt, B.J. (2005). Disrupting reconsolidation of drug memories reduces cocaine-seeking behaviour. Neuron, 47, 795-801.

Here, we show that infusion of Zif268 antisense oligodeoxynucleotides into the basolateral amygdala, prior to the reactivation of a well-learned memory for a conditioned stimulus (CS)-cocaine association, abolishes the acquired conditioned reinforcing properties of the drug-associated stimulus and thus its impact on the learning of a new cocaine-seeking response. Furthermore, we show that reconsolidation of CS-fear memories also requires Zif268 in the amygdala. These results demonstrate that appetitive CS-drug memories undergo reconsolidation in a manner similar to aversive memories and that this amygdala-dependent reconsolidation can be disrupted to reduce the impact of drug cues on drug seeking.
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[64.] Jm/Fragment 008 01 - Diskussion
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Information enters the trisynaptic one-way loop via the axons of the entorhinal cortex (EC; i.e., originating in layer II), known as perforant fibres (or the perforant path, given that it penetrates through the subiculum and the space that separates it from the dentate [gyrus).] Information enters this one-way loop via the axons of the entorhinal cortex, known as perforant fibres (or the perforant path, because it penetrates through the subiculum and the space that separates it from the dentate gyrus).
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[65.] Jm/Fragment 331 04 - Diskussion
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In the majority of human studies demonstrating an impairing effect of elevated cortisol on memory, the stressor or GC is applied before stimulus presentation and encoding, and recall is tested within 1-2 hours. In such a paradigm, cortisol levels are elevated during all memory phases (i.e., encoding, consolidation and retrieval). Disruption of any one of these memory processes could account for detrimental effects on memory and might obscure any facilitated process. In many of the human studies demonstrating an impairing effect of elevated cortisol on memory, the stressor or glucocorticoid is applied before stimulus presentation and learning, and recall is tested within 1–2 hr. In such a paradigm, cortisol levels are elevated during all memory phases: the learning period (initial encoding of the information), consolidation (the continuous transfer of information into longer term storage), and retrieval (recall of information from memory stores). Disruption of any one of these memory processes could account for detrimental effects of stress on memory and might also obscure any facilitated process.
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[66.] Jm/Fragment 332 10 - Diskussion
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In animal studies however, evidence suggests that while the amygdala is involved in conditioning, the hippocampus plays an important role in forming memories of contextual cues associated with the conditioning event (Phillips & LeDoux, 1994). Pugh and colleagues (1997) conditioned rats to an auditory cue while placed in a white cooler (i.e., context). A glucocorticoid antagonist administered prior to conditioning or immediately after did not affect auditory cue conditioning 24 later (i.e., freezing behaviour in response to tone in a novel environment). The treatment did, however, impair contextual fear conditioning (i.e., failing to freeze when put inside the cooler without a tone) in treated animals compared to vehicle-treated controls. Similar findings have been observed in relation to the effects of corticosteroids on spatial memory (e.g., Conrad et al., 1997). Importantly in this regard, spatial memory paradigms in animal research typically involve some form of associative learning. Generally, a behaviour is learned over several trials through operant conditioning (i.e., the location of food in a radial arm maze or escape routes). Successful recall of the learned behaviour then required memory for spatial information in these tasks, which some consider explicit (i.e., episodic memory). Evidence suggests that while the amygdala is involved with conditioning, the hippocampus plays an important role in forming memories of contextual cues associated with the conditioning event (Phillips & LeDoux, 1992, 1994). Pugh and colleagues thus conditioned rats to an auditory cue while placed in a white cooler (context). A glucocorticoid antagonist administered prior to conditioning or immediately after did not affect auditory cue conditioning 24 hours later (freezing behavior in response to tone in a novel environment). The treatment did, however, impair contextual fear conditioning (failing to freeze when put inside cooler without the tone) in treated animals compared to vehicle-treated controls (Pugh, Fleshner, & Rudy, 1997). [...]

[...]

Similar findings have been obtained on the effects of corticosteroids on spatial memory, as measured using different types of mazes. It should be noted that although these studies are typically distinguished from “associative learning” studies in the animal

[page 31]

literature, spatial memory paradigms in animal research typically involve some type of associative learning. Generally, a behavior is learned over several trials through operant conditioning (location of food in a radial arm maze or escape routes). Successful recall of the learned behavior then requires memory for spatial information in these tasks, which some consider explicit (episodic) memory.

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[67.] Jm/Fragment 287 01 - Diskussion
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[For example, using a radial arm maze with rats, systemic postreactivation injections of propranol were] effective at producing amnesia if the memory was first reactivated (Przybyslawski et al., 1999). Similarly, disruption of CREB-mediated transcription in the forebrain interferes with the reconsolidation of contextual fear memories (Kida et al., 2002). In support of the possibility that memories stored within the hippocampus itself might undergo reconsolidation are the findings showing that reactivation of contextual memories induces the expression of zif268, a gene implicated in the consolidation of new hippocampal-dependent memories (Hall et al., 2001). For example, using a radial arm maze, systemic postreactivation injections of propranol were effective at producing amnesia if the memory was first reactivated (Przybyslawski et al., 1999). [...] Similarly, recent findings that disruption of CREB-mediated transcription in the forebrain interferes with the reconsolidation of contextual fear memories (Kida et al., 2002) suffer from the same drawback. In support of the possibility that memories stored within the hippocampus itself might undergo reconsolidation are the recent findings showing that reactivation of contextual memories induces the expression of zif268, a gene implicated in consolidation of new hippocampal-dependent memories (Hall et al., 2001).
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[68.] Jm/Fragment 053 14 - Diskussion
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Human and animal studies firmly establish that the high levels of glucocorticoids released during stress impair the function of the hippocampus, thereby weakening or completely disrupting those aspects of contextual and episodic memory subserved by this structure. We reason herein that if stress interferes with the normal functions of the hippocampus, and the hippocampus is central to context effects in memory, then stress should interfere with those forms of memory dependent upon context and the binding it supports. Thus, we presently postulate that manipulations adversely affecting contextual encoding and retrieval, such as stress, should interfere with memory retrieval, [...] We argue that manipulations adversely affecting contextual encoding and retrieval should interfere with veridical remembering. Stress could be one such factor. [...] Human and animal studies firmly establish that the high levels of glucocorticoids released during stress impair the function of the hippocampus, weakening or completely disrupting those aspects of contextual and episodic memory subserved by this structure (De Quervain et al. 2000,Diamond and Rose 1994, Lupien et al. 1998, Nadel and Jacobs 1998, Newcomer et al. 1999).

We reasoned that if stress interferes with the normal functions of the hippocampus, and the hippocampus is central to context effects in memory, then stress might interfere with those forms of memory depending on context and the binding it supports.

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[69.] Jm/Fragment 351 01 - Diskussion
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We therefore reasoned that if stress interferes with the normal functions of the hippocampus, and the hippocampus is central to context effects in memory, then stress might interfere with those forms of memory depending on context and the binding it supports. We reasoned that if stress interferes with the normal functions of the hippocampus, and the hippocampus is central to context effects in memory, then stress might interfere with those forms of memory depending on context and the binding it supports.
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Cf. Jm/Fragment_053_14 where the same text has been used.

The copied text starts on the previous page: Jm/Fragment_350_20

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[70.] Jm/Fragment 345 01 - Diskussion
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[Further, gist-processing accounts of false recognition (Brainerd & Reyna, 1998; Schacter et al., 1998) assert that subjects] remember the gist of what they have experienced (i.e. the ‘theme’ of the word-list), rather than the specific details (i.e. the individual words). This reliance on gist leads naturally to false recognition of similar, but non-presented, words due to the high degree of semantic-relatedness between lures and presented words. Second, gist-processing accounts of false recognition (Brainerd and Reyna 1998, Schacter et al. 1998) assert that subjects remember the gist of what they have experienced (i.e. the ‘theme’ of the word-list), rather than the specific details (i.e. the individual words). This reliance on gist leads naturally to false recognition of similar, but non-presented, words because of the high degree of semantic-relatedness between lures and presented words.
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[71.] Jm/Fragment 034 01 - Diskussion
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Corticosteroid Receptors

Unlike the catecholamines, adrenocortical hormones pass readily through the blood-brain barrier (Roozendaal, Quirarte & McGaugh, 1997). Evidence suggests that corticosteroids have two methods of receptor activation (Lupien & McEwen, 1997). The first is genomic: once the hormone binds with the receptor, the receptor separates from its attached protein and moves into the cell nucleus, initiating transcription and mRNA protein synthesis. This genomic action eventually alters neuron receptor structure and activity, thus taking hours to weeks to induce an associated behavioral change (Sapolsky et al., 2000). The more rapid receptor activation involves corticosteroid interaction with the cell membrane, affecting transmitter response.

As previously discussed, the brain comprises two types of corticosteroid receptors relevant to stress research; mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs).


Lupien, S.J. & McEwen, B.S. (1997). The acute effects of corticosteroids on cognition: integration of animal and human model studies. Brain Research Reviews, 24, 1-27.

Sapolsky, R.L., Romero, M., & Munck, A.U. (2000). How Do Glucocorticoids Influence Stress Responses? Integrating Permissive, Suppressive, Stimulatory, and Preparative Actions. Endocrine Reviews, 21, 55–89.

Corticosteroid Receptors Unlike the catecholamines, adrenocortical hormones pass readily through the blood-brain barrier (Roosendaal, Quirarte, & McGaugh 1997). As Lupien & McEwen describe in their review (1997), evidence suggests that corticosteroids have two methods of receptor activation. The first is genomic: once the hormone binds with the receptor, the receptor separates from its attached protein and moves into the cell nucleus, initiating transcription and mRNA protein synthesis. This genomic action eventually alters neuron receptor structure and activity, thus taking hours to weeks to observe an associated behavioral change. The more rapid receptor activation involves corticosteroid interaction with the cell membrane, affecting transmitter response.

The brain has two types of corticosteroid receptors relevant to stress research: mineralocorticoid receptors and glucocorticoid receptors.


Lupien, S. J., & McEwen, B. S. (1997). The acute effects of corticosteroids on cognition: integration of animal and human model studies. Brain Research Review, 24, 1-27.

Roozendaal, B., Quirarte, G. L., & McGaugh, J. L. (1997). Stress-activated hormonal systems and the regulation of memory storage. In R. Yehuda & A. McFarlane (Eds.), Psychobiology of posttraumatic stress disorder (pp. 247-258). New York: Annals of the New York Academy of Sciences.

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[72.] Jm/Fragment 039 01 - Diskussion
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However, the findings for consolidation of verbal information are weak. One study suggested a facilitative effect of administered cortisol on consolidation of word recall when tested after a delay (Abercrombie et al., 2003), whereas others have found no difference between cortisol administration (de Quervain, Roozendaal, Nitsch, McGaugh & Hock, 2000) or stress (Wolf, Schommer, Hellhammer, Reischies & Kirschbaum, 2002) and controls. Thus, there is evidence for a facilitative effect of stress and cortisol on the consolidation of visual information, but little for verbal information.

Abercrombie, H.C., Kalin, N.H., Thurow, M.E., Rosenkranz, M.A., & Davidson, R.J. (2003). Cortisol variation in humans affects memory for emotionally laden and neutral information. Behavioral Neuroscience, 117, 505-516.

de Quervain, D.J., Roozendaal, B., Nitsch, R.M., McGaugh, J.L., & Hock C. (2000). Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 3, 313-314.

Wolf, O.T., Schommer, N., Hellhammer, D.H., Reischies, F.M., & Kirschbaum, C. (2002). Moderate psychosocial stress appears not to impair recall of words learned four weeks prior to stress exposure. Stress, 5, 59-64.

It is interesting to note, however, that of the several studies that have examined verbal memory by using the methodology described above, the findings for consolidation of verbal information are weak. One study suggested a facilitative effect of administered cortisol on consolidation of word recall when tested after a delay (Abercrombie et al., 2003), whereas others have found no difference between cortisol administration (de Quervain, Roozendaal, Nitsch, McGaugh, & Hock, 2000) or stress (Wolf, Schommer, Hellhammer, Reischies, & Kirschbaum, 2002) and controls. Thus, there is evidence for a facilitative effect of stress and cortisol on the consolidation of visual information, but little for verbal information.

Abercrombie, H. C., Kalin, N. H., Thurow, M. E., Rosenkranz, M. A., & Davidson, R. J. (2003). Cortisol variation in humans affects memory for emotionally laden and neutral information. Behavioral Neuroscience, 117, 505–516.

de Quervain, D. J., Roozendaal, B., Nitsch, R. M., McGaugh, J. L., & Hock, C. (2000). Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 3, 313– 314.

Wolf, O. T., Schommer, N. C., Hellhammer, D. H., Reischies, F. M., & Kirschbaum, C. (2002). Moderate psychosocial stress appears not to impair recall of words learned 4 weeks prior to stress exposure. Stress, 5, 59–64.

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[73.] Jm/Fragment 013 01 - Diskussion
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[These two pathways] have been heuristically related to spatial and nonspatial aspects of sensory input due to their preferential connections to parietal areas (i.e., the parahippocampal pathway) and inferior temporal areas (i.e., the perirhinal pathway), respectively. These two pathways have been heuristically characterized as relating to spatial and nonspatial aspects of sensory input because of their preferential connections to parietal areas (parahippocampal pathway) and inferior temporal areas (perirhinal pathway).
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[74.] Jm/Fragment 358 06 - Diskussion
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More specifically, while not interfering with memory for the individual items, which are represented in cortex, stress impairs the ability of the hippocampus to code the context, and to bind the items and context into a contextually-specific episode. Without the hippocampus acting as a contextual anchor, ‘true’ details are more easily confused with ‘false’ details of a similar appearance and nature. [page 8]

While not interfering with memory for the individual words, which are represented in cortex, stress impairs the ability of the hippocampus to code the spatial context, and to bind the words and specific details associated with the words into a contextually-specific episode.

[page 9]

Without the hippocampus acting as a spatial-contextual anchor, veridical details (such as the words themselves) are more easily confused with ‘false’ details (such as critical lures) of a similar appearance and nature.

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[75.] Jm/Fragment 052 01 - Diskussion
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[Also,] interference with memory destabilization both protected against the disruptive effects of protein synthesis inhibition and fixed the memory at the same strength despite additional learning. Thus, memory updating requires the destabilization of the original memory in order in integrate new information. Consequently, impairment of the restabilization process (e.g., through protein synthesis inhibition) affects not only the new information but also the reactivated memory, thereby leading to amnesia. Furthermore, interfering with memory

[page 8]

destabilisation both protected against the disruptive effects of protein synthesis inhibition and fixed the memory at the same strength in spite of further learning [20]. Therefore, memory updating requires the destabilisation of the original memory in order in integrate new information. As a result, impairment of the restabilisation process (e.g. through protein synthesis inhibition) affects not only the new information, but also the reactivated memory, thus leading to amnesia (Fig. 1C).


20. Lee JLC. Memory reconsolidation mediates the strengthening of memories by additional learning. Nat Neurosci. 2008; 11:1264–1266. [PubMed: 18849987]

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Providing succinct answers to such questions is integral given that the reconsolidation phase has been seized upon as crucial for the understanding of memory stability and, more recently, as a potential therapeutic target in the treatment of disorders such as post traumatic stress and drug addiction. Presently, little is known about the reactivation process, or what might be the adaptive function of retrieval-induced plasticity. Reconsolidation has long been proposed to mediate memory updating, but only recently has this hypothesis been supported experimentally. The reconsolidation phase has been seized upon as critical for the understanding of memory stability, and more recently as a potential therapeutic target in the treatment of disorders such as post-traumatic stress and drug addiction. However, little is known about the reactivation process, nor what might be the adaptive function of retrieval-induced plasticity. Reconsolidation has long been proposed to mediate memory updating, but only recently has this hypothesis been supported experimentally.
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[Similar to what has been found for Pavlovian conditioning (e.g.,] Nader et al., 2000), instrumental conditioning (e.g., Wang et al., 2005), and human procedural memory (Walker et al., 2003), reactivated episodic memories, in our study, underwent similar time-dependent reconsolidation processing. Similar to what has been found for Pavlovian conditioning (e.g., Nader et al. 2000), instrumental conditioning (e.g., Wang et al. 2005), and human procedural memory (Walker et al. 2003), reactivated episodic memories also undergo a time-dependent reconsolidation process:
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(Hindemith) Schumann

[78.] Jm/Fragment 343 09 - Diskussion
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Indeed, retrieving an episodic memory is largely a reconstructive act (Schacter & Tulving, 1994), and under some conditions this reconstruction can go awry. Our results suggest that correctly reconstructing an episode requires binding together the different elements of that episode, and as such depends integrally upon congruency between available contexts at encoding and retrieval. Retrieving an episodic memory is largely a reconstructive act (Schacter and Tulving 1994), and under some conditions this reconstruction can go awry. We suppose that correctly reconstructing an episode requires binding together the different elements of that episode (what was seen, heard, etc.), and that context plays a critical role in this binding process.
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(Hindemith) Agrippina1

[79.] Jm/Fragment 344 01 - Diskussion
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[Failure to bind properly leads to the possibility of incorrect retrieval and consequently, false memory. Our research has thus] targeted local context, via its role in episodic binding, and identified it as an important element in the understanding of memory distortions. Failure to bind properly leads to the possibility of incorrect retrieval and consequently, false memory. Our research starts from this set of assumptions and targets context, via its role in episodic binding, as an important element in the understanding of memory distortions.
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(Hindemith) Agrippina1

[80.] Jm/Fragment 344 14 - Diskussion
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Spreading activation theories of false recognition assert that exposure to a word causes the activation of semantically-related words (e.g., Collins & Loftus, 1975; Underwood, 1965). [...] Similarly, in terms of false recognition, presentation of an entire list of related words virtually guarantees that the critical lure will undergo considerable activation. An interpretation of such an effect pertains to an implicit associative response. Thus, activation of a nonpresented word may result in a sense of familiarity, or even the recollection that one actually encountered the word on the list when indeed they did not. Further, gist-processing accounts of false recognition (Brainerd & Reyna, 1998; Schacter et al., 1998) assert that subjects [remember the gist of what they have experienced (i.e. the ‘theme’ of the word-list), rather than the specific details (i.e. the individual words).] Spreading activation theories of false recognition assert that exposure to a word causes the activation of semantically related words (e.g. Collins and Loftus, 1975; Underwood, 1965). Presentation of an entire list of related words virtually guarantees that the critical lure will undergo considerable activation. This activation of a nonpresented word may result in a sense of familiarity, or even the recollection that one actually encountered the word on the list. [...]

Second, gist-processing accounts of false recognition (Brainerd and Reyna 1998, Schacter et al. 1998) assert that subjects remember the gist of what they have experienced (i.e. the ‘theme’ of the word-list), rather than the specific details (i.e. the individual words).

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(Hindemith) Agrippina1

[81.] Jm/Fragment 350 20 - Diskussion
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The literature indicates that hippocampus has a dense concentration of receptors for glucocorticoids (GCs), hormones released during stress (eg., McEwen et al., 1986). Further, human and animal studies firmly establish that the high levels of glucocorticoids released during stress impair the function of the hippocampus, thereby weakening or completely disrupting those aspects of contextual and episodic memory subserved by this structure (De Quervain et al., 2000; Nadel & Jacobs, [1998; Newcomer et al. 1999).] The hippocampus has a dense concentration of receptors for glucocorticoids, hormones released during stress (eg. McEwen et al. 1986 ). Human and animal studies firmly establish that the high levels of glucocorticoids released during stress impair the function of the hippocampus, weakening or completely disrupting those aspects of contextual and episodic memory subserved by this structure (De Quervain et al. 2000,Diamond and Rose 1994, Lupien et al. 1998, Nadel and Jacobs 1998, Newcomer et al. 1999).
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Sichter
(Hindemith) Agrippina1

[82.] Jm/Fragment 037 14 - Diskussion
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Studies with corticosteroid receptor agonists and antagonists suggest that low levels of corticosteroids (in which MRs are fully occupied) may influence attention to encoding of relevant stimuli, while increasing levels associated with stress (in which GRs start to become occupied) act on consolidation processes (with moderate doses facilitating memory and very high doses impairing it). Thus the majority of human studies, in attempting to approximate moderate stress, may be raising cortisol levels beyond the peak of the inverted-U, thereby resulting in detrimental effects on memory. Animal studies showing a facilitative effect of stress-levels of corticosterone on memory may instead be achieving the peak for those species. Clearly more research on dose-dependent effects in humans is needed to shed light on this issue. Studies with corticosteroid receptor agonists and antagonists suggest that low levels of corticosteroids (in which mineralocorticoid receptors are fully occupied) may influence attention and encoding of

[page 50]

relevant stimuli, while increasing levels associated with stress (in which glucocorticoid receptors start to become occupied) act on consolidation processes (with moderate doses facilitating memory and very high doses impairing it).

[...]

Thus the majority of human studies reviewed above, in attempting to approximate moderate stress, may be raising cortisol levels beyond the peak of the inverted-U, resulting in detrimental effects on memory. Animal studies showing a facilitative effect of stress-levels of corticosterone on memory may instead be achieving the peak for those species. Clearly more research on dose-dependent effects in humans is needed to shed light on this issue.

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Sichter
(Hindemith) Agrippina1

[83.] Jm/Fragment 039 09 - Diskussion
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These studies provide stronger evidence of encoding and consolidation effects of stress, although the findings are mixed. While one study found a detrimental effect on verbal memory (Lupien et al., 1995), several others found a facilitative effect on visual memory (Buchanan & Lovallo, 2001; Abercrombie et al., 2003; Cahill et al., 2003). These studies (with the exception of Cahill et al., 2003), however, continue to conflate encoding and consolidation processes. Studies examining attentional effects have generally found that stress and cortisol interfere with selective attention and working memory. Furthermore, none of these studies manipulated either stress or cortisol levels on the day of memory testing in order to determine retrieval effects. Only one human study (de Quervain et al., 2000) and two animal studies (de Quervain et al., 1998; Oitzl & De Kloet, 1992) have directly tested for the effects of stress during each stage of memory formation and recall. These researchers found evidence of impaired retrieval. These studies provide stronger evidence of encoding and consolidation effects of stress, although the findings are mixed. While one study found a detrimental effect on verbal memory (Lupien et al., 1995), several others found a facilitative effect on visual memory (Buchanan & Lovallo, 2001; Abercrombie et al., 2003; Cahill et al., 2003). These studies (with the exception of Cahill et al. 2003), however, continue to conflate encoding and consolidation processes. Studies examining attentional effects have generally found stress and cortisol to interfere with selective attention and working memory. In addition, none of the studies cited above manipulated stress or cortisol levels on the day of memory testing to investigate retrieval effects. Only one human study (de Quervain et al., 2000) and two animal studies (de Quervain et al., 1998; Oitzl & De Kloet, 1992) have directly tested for the effects of stress during each stage of memory formation and recall. These researchers found evidence of impaired retrieval.
Anmerkungen

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Sichter
(Hindemith) Agrippina1

[84.] Jm/Fragment 241 10 - Diskussion
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Functional brain imaging studies have further shown that medial temporal, parietal and prefrontal cortices are involved in recognition memory of prior episodes (Rugg & Wilding, 2000; Rugg & Yonelinas, 2003). The functional role that these regions play in memory retrieval, however, is still debated. Specifically, it is unclear whether recollection, the retrieval of specific context-based information about a past experience, and familiarity, an acontextual sense that an event has been previously experienced (Tulving, 1985), are mediated by dissociated neural systems or separate strong (i.e., remote) memories from weak (i.e., recent) memories. Some studies suggest that separate cortical networks (Yonelinas et al., 2005) and differential activation in the parietal cortex (Vilberg & Rugg, 2007) mediate these two distinct memory processes, whereas other studies suggest that recollection and familiarity reflect differences in the strength of a common memory trace (Donaldson, 1996; Dunn, 2004; Gonsalves et al., 2005; Squire et al., 2007; Wixted, 2007). Yago and Ishai (2006) found that activation elicited by new paintings in the parietal cortex was reduced with decreased similarity to old items, whereas in the hippocampus and precuneus, stronger responses were evoked by new, visually different paintings.

Donaldson, W. (1996). The role of decision processes in remembering and knowing. Memory and Cognition, 14, 523–533.

Dunn J. C. (2004). Remember-know: a matter of confidence. Psychological Review, 111, 524–54210 [sic].

Gonsalves, B.D., Kahn I., Curran, T., Norman, K.A., & Wagner A.D. (2005). Memory strength and repetition suppression: multimodal imaging of medial temporal cortical contributions to recognition. Neuron, 47, 751–761.

Rugg, M.D. & Wilding, E.L. (2000). Retrieval processing and episodic memory: electrophysiological and neuroimaging evidence. Trends in Cognitive Sciences, 4, 108-115.

Rugg, M.D. & Yonelinas, A.P. (2003). Human recognition memory: a cognitive neuroscience perspective. Trends in Cognitive Sciences, 7, 313–319.

Squire, L.R., Wixted, J.T., & Clark, R.E. (2007). Recognition memory and the medial temporal lobe: a new perspective. Nature Reviews Neuroscience, 8, 872–883.

Tulving, E. (1985). Memory and consciousness. Canadian Psychology, 26, 1–12.

Vilberg, K.L. & Rugg, M.D. (2007). Dissociation of the neural correlates of recognition memory according to familiarity, recollection, and amount of recollected information. Neuropsychologia, 45(10), 2216-2225.

Wixted, J.T. (2007). Dual-process theory and signal-detection theory of recognition memory. Psychological Review, 114, 152–176.

Yago, E. & Ishai, A. (2006). Recognition memory is modulated by visual similarity. Neuroimage, 31, 807–817.

Yonelinas, A.P., Otten, L.J., Shaw, K.N., & Rugg, M.D. (2005). Separating the brain regions involved in recollection and familiarity in recognition memory. Journal of Neuroscience, 25, 3002–3008.

Functional brain imaging studies have shown that medial temporal, parietal and prefrontal cortices are involved in recognition memory of prior episodes (Rugg and Wilding, 2000; Rugg and Yonelinas, 2003). The functional role that these regions play in memory retrieval, however, is still debated. Specifically, it is unclear whether recollection, the retrieval of specific information about a past experience, and familiarity, a sense that an event has been previously experienced (Tulving, 1985), are mediated by dissociated neural systems or separate strong memories from weak memories. Some studies suggest that separate cortical networks (Yonelinas et al., 2005) and differential activation in parietal cortex (Vilberg and Rugg, 2007) mediate these two distinct memory processes, whereas other studies suggest that recollection and familiarity reflect differences in the strength of a common memory trace (Donaldson, 1996; Dunn, 2004; Gonsalves et al., 2005; Squire et al., 2007; Wixted, 2007).

[...] Moreover, activation elicited by new paintings in parietal cortex was reduced with decreased similarity to the old items, whereas in the hippocampus and precuneus, stronger responses were evoked by the new, visually different paintings.


Donaldson, W. (1996). The role of decision processes in remembering and knowing. Mem. Cogn. 14, 523–533.

Dunn, J. C. (2004). Remember-know: a matter of confidence. Psychol. Rev. 111, 524–542.

Gonsalves, B. D., Kahn, I., Curran, T., Norman, K. A., and Wagner, A. D. (2005). Memory strength and repetition suppression: multimodal imaging of medial temporal cortical contributions to recognition. Neuron 47, 751–761.

Rugg, M. D., and Wilding, E. L. (2000). Retrieval processing and episodic memory. Trends Cogn. Sci. 4, 108–115.

Rugg, M. D., and Yonelinas, A. P. (2003). Human recognition memory: a cognitive neuroscience perspective. Trends Cogn. Sci. 7, 313–319.

Squire, L. R., and Bayley, P. J. (2007). The neuroscience of remote memory. Curr. Opin. Neurobiol. 17, 185–196.

Squire, L. R., Wixted, J. T., and Clark, R. E. (2007). Recognition memory and the medial temporal lobe: a new perspective. Nat. Rev. Neurosci. 8, 872–883.

Vilberg, K. L., and Rugg, M. D. (2007). Dissociation of the neural correlates of recognition memory according to familiarity, recollection, and amount of recollected information. Neuropsychologia 45, 2216–2225.

Yonelinas, A. P., Otten, L. J., Shaw, K. N., and Rugg, M. D. (2005). Separating the brain regions involved in recollection and familiarity in recognition memory. J. Neurosci. 25, 3002–3008

Wixted, J. T. (2007). Dual-process theory and signal-detection theory of recognition memory. Psychol. Rev. 114, 152–176.

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Sichter
(Graf Isolan) Singulus

[85.] Jm/Fragment 332 01 - Diskussion
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Pharmacological functional magnetic resonance imaging studies have recently shown that this effect is dependent on β-adrenergic activation in the amygdala (Strange & Dolan, 2004; van Stegeren et al., 2005), thereby replicating the effects demonstrated in rats (McGaugh & Roozendaal, 2002; Roozendaal, 2002). However, the role of the amygdala in emotional memory retrieval is not as well understood (Taylor et al., 1998; Dolan et al., 2000; Smith et al., 2004; Strange & Dolan, 2004). More imaging studies are warranted that investigate the effects of stress or stress hormones on memory retrieval. The only study on this topic to date in humans observed a reduced blood flow in the right posterior medial temporal lobe following cortisol treatment (de Quervain et al., 2003).

de Quervain, D.J., Henke, K., Aerni, A., Treyer, V., McGaugh, J.L., Berthold, T., Nitsch, R.M., Buck, A., Roozendaal, B., & Hock, C. (2003). Glucocorticoid-induced impairment of declarative memory retrieval is associated with reduced blood flow in the medial temporal lobe. European Journal of Neuroscience, 17, 1296–1302.

McGaugh, J. L. & Roozendaal, B. (2002). Role of adrenal stress hormones in forming lasting memories in the brain. Current Opinion in Neurobiology, 12(2), 205-210.

Roozendaal, B. (2002). Stress and memory; Opposing effects of glucocorticoids on memory consolidation and retrieval. Neurobiology of Learning and Memory, 78, 578-595.

Roozendaal, B. (2002). Stress and memory: opposing effects of glucocorticoids on memory consolidation and memory retrieval. Neurobiology of Learning and Memory, 78, 578-595.

Smith, D.M., Wakeman, D., Patel, J., & Gabriel, M. (2004). Fornix lesions impair context-related cingulothalamic neuronal patterns and concurrent discrimination learning. Behavioural Neuroscience, 118, 1225–1239.

Pharmacological functional magnetic resonance imaging studies have shown recently that this effect is dependent on β-adrenergic activation in the amygdala (Strange and Dolan, 2004; van Stegeren et al., 2005), thereby replicating the effects demonstrated in rats (McGaugh and Roozendaal, 2002; Roozendaal, 2002). However, the role of the amygdala in emotional memory retrieval is not as well understood (Taylor et al., 1998; Dolan et al., 2000; Smith et al., 2004; Strange and Dolan, 2004). More imaging studies are warranted that investigate the effects of stress or stress hormones on memory retrieval. The only study on this topic to date observed a reduced blood flow in the right posterior medial temporal lobe after cortisol treatment (de Quervain et al., 2003).

de Quervain DJ, Henke K, Aerni A, Treyer V, McGaugh JL, Berthold T, Nitsch RM, Buck A, Roozendaal B, Hock C (2003) Glucocorticoid-induced impairment of declarative memory retrieval is associated with reduced blood flow in the medial temporal lobe. Eur J Neurosci 17:1296–1302.

Dolan RJ, Lane R, Chua P, Fletcher P (2000) Dissociable temporal lobe activations during emotional episodic memory retrieval. NeuroImage 11:203–209.

McGaugh JL, Roozendaal B (2002) Role of adrenal stress hormones in forming lasting memories in the brain. Curr Opin Neurobiol 12:205–210.

Roozendaal B (2002) Stress and memory: opposing effects of glucocorticoids on memory consolidation and memory retrieval. Neurobiol Learn Mem 78:578–595.

Smith AP, Henson RN, Dolan RJ, Rugg MD (2004) fMRI correlates of the episodic retrieval of emotional contexts. NeuroImage 22:868–878.

Strange BA, Dolan RJ (2004) β-adrenergic modulation of emotional memory-evoked human amygdala and hippocampal responses. Proc Natl Acad Sci USA 101:11454–11458.

Taylor SF, Liberzon I, Fig LM, Decker LR, Minoshima S, Koeppe RA (1998) The effect of emotional content on visual recognition memory: a PET activation study. NeuroImage 8:188–197.

van Stegeren AH, Goekoop R, Everaerd W, Scheltens P, Barkhof F, Kuijer JP, Rombouts SA (2005) Noradrenaline mediates amygdala activation in men and women during encoding of emotional material. NeuroImage 24:898–909.

Anmerkungen

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Sichter
(Graf Isolan) Agrippina1

[86.] Jm/Fragment 035 01 - Diskussion
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[These corticosteroid receptors comprise different affinities for endogenous and] synthetic corticosteroids and vary in their distribution in the brain. Both, however, are found extensively in the hippocampus. Recent theoretical and experimental work suggests that the way these receptors function and interact might explain the varied and sometimes inconsistent relationship between corticosteroids and cognition (Lupien & McEwen, 1997; De Kloet, Oitzl & Joels, 1999; Roozendaal, 1999. The MRs are found predominantly in the hippocampus, with some expression in other limbic and brainstem nuclei (McEwen, de Kloet & Rostene, 1986). MRs bind to cortisol (in humans) and corticosterone (in rodents) with high affinity, and are thus largely occupied under non-stressful conditions when corticosteroid levels are low (see McEwen et al., 1986, for review). MR activation via low levels of corticosteroids generally results in reduced calcium currents and thus more stable responses to excitatory glutamatergic and biogenic amine inputs. This has lead some to suggest that activation of MRs play a role in maintaining homeostasis (De Kloet et al., 1999).

Glucocorticoid receptors have one-tenth the affinity for cortisol and corticosterone (Reul & de Kloet, 1985). Thus as endogenous corticosteroid levels rise under stress and most of the MRs become occupied, GRs gradually become activated. If the stressor is moderate to severe (or a corticosteroid is administered in comparable levels), the percentage of GR occupation increases substantially. GRs are distributed widely throughout the brain, including the limbic system, brainstem, hypothalamic nuclei, and cortex, although they are most concentrated in the hippocampus (McEwen, Weiss, & Schwartz, 1968). GR activation leads to enhanced calcium currents and responsiveness to excitatory neurotransmitters. This activation is generally followed by a decrease in cellular activity, helping to restore cells to their homeostatic state (De Kloet et al., 1999). There is evidence, however, that the increase in excitatory activity associated with GR activation can lead to neuron atrophy and death in the hippocampus (see below for further discussion).


de Kloet, E.R., Oitzl, M.S., & Joëls, M. (1999). Stress and cognition: Are corticosteroids good or bad guys? Trends in Neuroscience, 22, 422-426.

Lupien, S.J. & McEwen, B.S. (1997). The acute effects of corticosteroids on cognition: integration of animal and human model studies. Brain Research Reviews, 24, 1-27.

McEwen, B.S., De Kloet, E.R., & Rostene, W. (1986). Adrenal steroid receptors and actions in the nervous system. Physiological Reviews, 66, 1121–1188.

McEwen, B.S., Weiss, J.M., & Schwartz, L.S. (1968). Selective retention of corticosterone by limbic structure in rat brain. Nature, 220, 911-912.

Reul, J.M.H.M. & De Kloet, E.R. (1985). Two receptor systems for corticosterone in ratbrain: microdistribution and differential occupation. Endocrinology, 117, 2505-2512

Roozendaal, B. (1999). Glucocorticoids and the regulation of memory consolidation. Psychoneuroendocrinology, 25, 213-238.

[These corticosteroid receptors] have different affinities for endogenous and synthetic corticosteroids and vary in their distribution in the brain. Both, however, are found extensively in the hippocampus. Recent theoretical and experimental work suggests that the way these receptors function and interact might explain the varied and sometimes inconsistent relationship between corticosteroids and cognition (Lupien & McEwen, 1997; De Kloet, Oitzl, & Joels, 1999; Roozendaal, 1999).

The mineralocorticoid receptors (MRs) are found largely in the hippocampus, with some expression in other limbic and brainstem nuclei (McEwen, de Kloet, & Rostene, 1986). MRs bind to cortisol (in humans) and corticosterone (in rodents) with high affinity, and are thus largely occupied under non-stressful conditions when corticosteroid levels are low (see McEwen, et al., 1986, for review). MR activation via low levels of corticosteroids generally results in reduced calcium currents and thus more stable responses to excitatory glutamatergic and biogenic amine inputs. This has lead some to suggest that activation of MRs play a role in maintaining homeostasis (De Kloet et al., 1999).

Glucocorticoid receptors (GRs) have one-tenth the affinity for cortisol and corticosterone (Reul & de Kloet, 1985). Thus as endogenous corticosteroid levels rise under stress and most of the MRs become occupied, GRs gradually become activated. If the stressor is moderate to severe (or a corticosteroid is administered in comparable levels), the percentage of GR occupation increases substantially. GRs are distributed widely throughout the brain, including the limbic system, brainstem, hypothalamic nuclei, and cortex, although they are most concentrated in the hippocampus (McEwen, Weiss, & Schwartz, 1968). GR activation leads to enhanced calcium currents and responsiveness to excitatory neurotransmitters. This activation is generally followed by a decrease in cellular activity, helping to restore cells to their homeostatic state (De Kloet et al., 1999). There is evidence, however, that the increase in excitatory activity associated with GR activation can lead to neuron atrophy and death in the hippocampus (see section below).


De Kloet, E. R., Oitzl, M. S., & Joels, M. (1999). Stress and cognition: Are orticosteroids good or bad guys? Trends in Neuroscience, 22, 422-426.

Lupien, S. J., & McEwen, B. S. (1997). The acute effects of corticosteroids on cognition: integration of animal and human model studies. Brain Research Review, 24, 1-27.

McEwen, B. S., De Kloet, E. R., & Rostene, W. H. (1986). Adrenal steroid receptors and actions in the nervous system. Physiology Review, 66, 1121-1188.

McEwen, B. S., Weiss, J. M., & Schwartz, L. S., 1968. Selective retention of corticosterone by limbic structures in rat brain. Nature, 220, 911-912.

Reul, J. M. H. M., & De Kloet, E. R. (1985). Two receptor systems for corticosterone in rat brain: microdistribution and differential occupation. Endocrinology, 117, 2505-2512.

Roozendaal, B. (2000 [sic!]). Glucocorticoids and the regulation of memory consolidation. Psychoneuroendocrinology, 25, 213-238.

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Sichter
(Graf Isolan) Agrippina1

[87.] Jm/Fragment 033 01 - Diskussion
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[While cortisol works to make energy available, it also contributes to the] shut-down of bodily activities that compete for resources—longer-term processes or maintenance activities that can be delayed until after the stressful situation subsides. These include immune function, tissue repair, digestion and energy storage, and certain reproductive activities (Sapolsky et al., 2000). Elevated levels of cortisol eventually trigger a negative feedback inhibition process to ensure hormone levels are prevented from rising out of control. High levels of cortisol thus signal the hypothalamus to stop releasing CRF, essentially down-shifting the HPA response. This maintains cortisol at the level necessary to cope with the stressor, or returns cortisol levels to their basal level once the stressor has passed (Bullock, 2001).

Sapolsky, R.L., Romero, M., & Munck, A.U. (2000). How Do Glucocorticoids Influence Stress Responses? Integrating Permissive, Suppressive, Stimulatory, and Preparative Actions. Endocrine Reviews, 21, 55–89.

[Page 11]

While cortisol works to make energy available, it also contributes to the shut-down of bodily activities that compete for resources—longer-term “building projects” or maintenance activities that can be delayed until after the emergency. These include immune function, tissue repair, digestion and energy storage, and certain reproductive activities (Bullock, 2001).

[Page 12]

Elevated levels of cortisol eventually trigger a negative feedback inhibition process to keep hormone levels from rising out of control. High levels of cortisol thus signal the hypothalamus to stop releasing CRF, essentially down-shifting the HPA response. This maintains cortisol at the level necessary to cope with the stressor, or returns cortisol levels to their basal level once the stressor has passed (Bullock, 2001).


Bullock, K. (2001) Regional neural regulation of immunity: Anatomy and function. In B. S. McEwen (Vol. Ed.) & H. M. Goodman (Section Ed.), Handbook of physiology, Section 7: The endocrine system, Vol IV. New York: Oxford University Press.

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(Graf Isolan), Hindemith

[88.] Jm/Fragment 032 01 - Diskussion
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Glucocorticoids such as cortisol play an integral role in raising circulating levels of glucose in the blood to provide muscles and the brain energy for the stress response. Cortisol does this by stimulating the liver to convert glycogen into glucose (which is then released into the blood), inhibiting the secretion of insulin (which takes up glucose for storage), and promoting hepatic gluconeogenesis (converting amino acids into glucose when carbohydrate sources are depleted; Sherwood, 1997). Cortisol also promotes the break-down of protein (i.e., muscle) into amino acids for later gluconeogensis, and fat into fatty acids to provide an additional source of energy for some tissues (although the brain can only use glucose; Sherwood, 1997).

Sherwood, L. (1997). Human Physiology: from Cells to Systems. Belmont, CA: Wadsworth Publishing Company.

As the name implies, glucocorticoids such as cortisol play a critical role in raising circulating levels of glucose in the blood to provide muscles and the brain energy for the stress response. Cortisol does this by stimulating the liver to convert glycogen into glucose (which is then released into the blood), inhibiting the secretion of insulin (which takes up glucose for storage), and promoting hepatic gluconeogenesis (converting amino acids into glucose when carbohydrate sources are depleted) (Sherwood, 1997). Cortisol also promotes the break-down of protein (muscle) into amino acids for later gluconeogensis, and fat into fatty acids to provide an additional source of energy for some tissues (although the brain can only use glucose) (Sherwood, 1997).

Sherwood, L. (1997). Human Physiology: From Cells to Systems. Belmont, CA: Wadsworth Publishing Company.

Anmerkungen

Nothing has been marked as a citation.

Sichter
(Graf Isolan) Agrippina1

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Participants were exposed to the Trier Social Stress Test (TSST; Kirschbaum et al., 1993) or a non-stressful filler task after which they had to listen to 20 DRM word lists, each [followed by a computerized recognition task. Compared to controls, participants exposed to the TSST showed elevated rates of false recognition for the critical lures.] In a study by Payne et al. (2002), participants were exposed to the Trier Social Stress Test (TSST; Kirschbaum et al., 1993) or a non-stressful filler task after which they had to listen to 20 DRM word lists, each followed by a computerized recognition task. Compared to controls, participants exposed to the TSST showed elevated rates of false recognition for the critical lures.
Anmerkungen

The source is only mentioned in the next paragraph without apparent reference to this paragraph.

Sichter
(Hindemith) Agrippina1

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Researchers have also recently attempted to parse the effects of glucocorticoids on retrieval processes separate from learning and consolidation, and findings provide some support for Roozendaal’s (2002) theory that retrieval is impaired by stress. These studies present the stimuli to be learned in the first session under basal conditions and then apply the stressor or glucocorticoid just before retrieval on a subsequent session.

Roozendaal, B. (2002). Stress and memory; Opposing effects of glucocorticoids on memory consolidation and retrieval. Neurobiology of Learning and Memory, 78, 578-595.

Roozendaal, B. (2002). Stress and memory: opposing effects of glucocorticoids on memory consolidation and memory retrieval. Neurobiology of Learning and Memory, 78, 578-595.

Researchers have also recently attempted to parse the effects of glucocorticoids on retrieval processes separate from learning and consolidation, and findings provide some support for Roozendaal’s (2002) theory that retrieval is impaired by stress. These studies present the stimuli to be learned in the first session under basal conditions and then apply the stressor or glucocorticoid just before retrieval on a subsequent session.

Roozendaal, B. (2002). Stress and memory: Opposing effects of glucocorticoids on memory consolidation and memory retrieval. Neurobiology of Learning and Memory, 78, 578–595.

Anmerkungen

Though identical, the source is named only in the next paragraph, on the following page without apparent relation to the text documented here.

Sichter
(Graf Isolan), Hindemith

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[Using this type of] design, de Quervain, Roozendaal and McGaugh (1998) found that both shock and glucocorticoids administered just before retention testing impaired retrieval of spatial information in rats. Two pharmacological studies in humans have also shown an impairing effect of elevated cortisol on the retrieval of words learned 24 hr before (de Quervain et al., 2000, 2003), and Kuhlmann, Piel and Wolf (2005) similarly found that a psychosocial stressor impaired recall of both positive and negative (but not neutral) words. Wolf and colleagues (2002), however, found no effect of a stressor on retrieval of words learned 4 weeks earlier compared with controls.

de Quervain, D.J., Henke, K., Aerni, A., Treyer, V., McGaugh, J.L., Berthold, T., Nitsch, R.M., Buck, A., Roozendaal, B., & Hock, C. (2003). Glucocorticoid-induced impairment of declarative memory retrieval is associated with reduced blood flow in the medial temporal lobe. European Journal of Neuroscience, 17, 1296–1302.

de Quervain, D.J., Roozendaal, B., & McGaugh, J.L. (1998). Stress and glucocorticoids impair retrieval of long-term spatial memory. Nature, 394, 787-790.

de Quervain, D.J., Roozendaal, B., Nitsch, R.M., McGaugh, J.L., & Hock C. (2000). Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 3, 313-314.

Kuhlmann, S., Piel, M., & Wolf, O.T. (2005b). Impaired memory retrieval after psychosocial stress in healthy young men. Journal of Neuroscience, 25, 2977–2982.

Wolf, O.T., Schommer, N., Hellhammer, D.H., Reischies, F.M., & Kirschbaum, C. (2002). Moderate psychosocial stress appears not to impair recall of words learned four weeks prior to stress exposure. Stress, 5, 59-64.

Using this type of design, de Quervain, Roozendaal, and McGaugh (1998) found that both shock and glucocorticoids administered just before retention testing impaired retrieval of spatial information in rats. Two pharmacological studies in humans have also shown an impairing effect of elevated cortisol on the retrieval of words learned 24 hr before (de Quervain et al., 2000, 2003), and Kuhlmann, Piel, and Wolf (2005) similarly found that a psychosocial stressor impaired recall of both positive and negative (but not neutral) words. Wolf et al. (2002), however, found no effect of a stressor on retrieval of words learned 4 weeks earlier compared with controls.

de Quervain, D. J., Henke, K., Aerni, A., Treyer, V., McGaugh, J. L., Berthold, T., et al. (2003). Glucocorticoid-induced impairment of declarative memory retrieval is associated with reduced blood flow in the medial temporal lobe. European Journal of Neuroscience, 17, 1296–1302.

de Quervain, D. J., Roozendaal, B., & McGaugh, J. L. (1998, August 20). Stress and glucocorticoids impair retrieval of long-term spatial memory. Nature, 394, 787–790.

de Quervain, D. J., Roozendaal, B., Nitsch, R. M., McGaugh, J. L., & Hock, C. (2000). Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 3, 313–314.

Kuhlmann, S., Piel, M., & Wolf, O. T. (2005). Impaired memory retrieval after psychosocial stress in healthy young men. Journal of Neuroscience, 25, 2977–2982.

Wolf, O. T., Schommer, N. C., Hellhammer, D. H., Reischies, F. M., & Kirschbaum, C. (2002). Moderate psychosocial stress appears not to impair recall of words learned 4 weeks prior to stress exposure. Stress, 5, 59–64.

Anmerkungen

Word for word from the paper by Beckner et al. (2006). Nothing has been marked as a citation. Starting the next paragraph the source is named for the first time, though in that paragraph the text presented is from the original thesis of Beckner (2004). Thus again the origin of texts is obscured.

Sichter
(Graf Isolan) Agrippina1

[92.] Jm/Fragment 287 22 - Diskussion
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Cai and colleagues (2006) reported that when glucocorticoids were administered immediately after reactivation of a contextual fear memory, subsequent recall was significantly diminished. However, the effect of postreactivation glucocorticoid on contextual fear memory was reversed by a reminder shock, thereby suggesting that augmentation of single- [page 288] trial contextual fear memory extinction is the more likely mechanism for these effects of postreactivation corticosterone on subsequent memory (Cai et al., 2006). Cai et al. (2006) reported that when glucocorticoids are administered immediately after reactivation of a contextual fear memory, subsequent recall is significantly diminished. However, the effect of postreactivation glucocorticoid on contextual fear memory is reversed by a reminder shock. This finding suggests that augmentation of single-trial contextual fear memory extinc-

[page 5608]

tion is the more likely mechanism for the effects of postreactivation corticosterone on subsequent memory (Cai et al., 2006).

Anmerkungen

The source is not mentioned in the context of this text fragment.

Continued on the next page: Jm/Fragment_288_01

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(Hindemith) Agrippina1

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[However, the effect of postreactivation glucocorticoid on contextual fear memory was reversed by a reminder shock, thereby suggesting that augmentation of single-] trial contextual fear memory extinction is the more likely mechanism for these effects of postreactivation corticosterone on subsequent memory (Cai et al., 2006). Maroun and Akirav (2008), however, provided evidence that stress might have an inhibitory effect on the reconsolidation of recognition memory. They found that in habituated (i.e., high arousal level) and nonhabituated (i.e., low arousal level) rats, exposure to an out-of-context stressor impaired long-term reconsolidation of object recognition memory. Further, Zhao and colleagues (2007) were the first to demonstrate that cocaine-conditioned place preference (i.e., context cue memory) was blocked in rats experiencing stress following re-exposure to the previously drug-paired chamber, thereby demonstrating a potential inhibitory effect of stress on the reconsolidation of contextually mediated drug memory.

Extensive evidence suggests that the basolateral amygdala (BLA) is a key region that regulates the effects of stress and glucocorticoids on memory formation, consolidation and reconsolidation (Roozendaal & McGaugh, 1997; Roozendaal et al., 2002; Roozendaal, 2003). Lesions of the BLA block the dexamethasone-induced memory enhancement in an inhibitory avoidance task, suggesting that the BLA is a critical site for the modulatory effect of glucocorticoids on memory formation (Roozendaal & McGaugh, 1996). It has been reported that glucocorticoids in BLA contribute to memory consolidation. Post-training infusions of a GR agonist into the BLA enhance memory performance (Roozendaal & McGaugh, 1997). Immediate postretrieval intra-BLA infusion of RU486 selectively impairs long-term auditory fear memory, suggesting that glucocorticoid receptors in the BLA are required for reconsolidation of auditory fear memory (Jin et al., 2007). Wang and colleagues (2008) also demonstrated that a GR antagonist infused into the BLA reversed the inhibitory effect of post-reactivation stress on a morphine reward memory. This finding suggests that activation of GRs in the BLA plays a critical role in the effects of postreactivation stress on context-cue dependent drug-related memory.

However, the effect of postreactivation glucocorticoid on contextual fear memory is reversed by a reminder shock. This finding suggests that augmentation of single-trial contextual fear memory extinc-

[page 5608]

tion is the more likely mechanism for the effects of postreactivation corticosterone on subsequent memory (Cai et al., 2006). Maroun and Akirav (2008) provided the first evidence that stress might have an inhibitory effect on the reconsolidation of memory. They found that in habituated (high arousal level) and nonhabituated (low arousal level) rats, exposure to an out-of-context stressor impaired long-term reconsolidation of objective recognition memory (Maroun and Akirav, 2007).

Our previous study was the first to demonstrate that cocaine CPP was blocked in rats experiencing stress after re-exposure to the previously drug-paired chamber, showing a potential inhibitory effect of stress on reconsolidation of drug-related memory (Zhao et al., 2007). [...]

[...]

Likewise, extensive evidence suggests that the BLA is a key region that regulates the effects of stress and glucocorticoids on memory formation, consolidation, and reconsolidation (Roozendaal and McGaugh, 1997; Roozendaal et al., 2002; Roozendaal, 2003). Lesions of the BLA, but not the CeA, block the dexamethasone-induced memory enhancement in an inhibitory avoidance task, suggesting that the BLA is a critical site for the modulatory effect of glucocorticoids on memory formation (Roozendaal and McGaugh, 1996). It has been reported that glucocorticoids in BLA, but not the CeA, contribute to memory consolidation. Post-training infusions of a GR agonist into the BLA, but not into the CeA, enhance memory performance (Roozendaal and McGaugh, 1997). Immediate postretrieval intra-BLA infusion of RU486 selectively impairs long-term auditory fear memory, suggesting that glucocorticoid receptors in the BLA are required for reconsolidation of auditory fear memory (Jin et al., 2007).

Consistent with previous studies, we showed that aGR agonist injected into the BLA, but not into the CeA, after memory reactivation mimics the effects of postreactivation stress. Moreover, we demonstrated that a GR antagonist infused into the BLA, but not into the CeA, reversed the inhibitory effect of postreactivation stress on a morphine reward memory. This finding suggests that activation of GRs in the BLA plays a critical role in the effects of postreactivation stress on drug-related memory.

Anmerkungen

It is clear to the reader that here the research of others is presented including the research of Wang et al. (2008). It is not clear however, that this presentation is taken from Wang et al. (2008) in its entirety, only making minor adjustments.

Sichter
(Hindemith) Agrippina1

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Morphine CPP is persistently disrupted when anisomycin, a protein synthesis inhibitor, is administered after a conditioning session (Milekic et al., 2006). When mice previously conditioned for cocaine place preference are re-exposed to cocaine in the drug-paired compartment after systemic administration of SL327, an inhibitor of ERK (extracellular signal-regulated protein kinase) activation, CPP response is abolished (Valjent et al., 2006). Together, drug-related memory can be inhibited or erased by interrupting its reconsolidation process. Morphine CPP is persistently disrupted when anisomycin, a protein synthesis inhibitor, is administered after a conditioning session (Milekic et al., 2006). When mice previously conditioned for cocaine place preference are re-exposed to cocaine in the drug-paired compartment after systemic administration of SL327 [α-[amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl) benzeneacetonitrile], an inhibitor of ERK (extracellular signal-regulated protein kinase) activation, CPP response is abolished (Valjent et al., 2006a). Together, drug-related memory can be inhibited or erased by interrupting its reconsolidation process.
Anmerkungen

The source is not mentioned here, only on the next page in a different context.

Sichter
(Hindemith) Agrippina1

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Beckner and colleagues (2006) recently addressed these discrepant findings by attempting to parse the effects of an acute psychosocial stressor on these separate memory processes by varying the timing of the stressor. The psychosocial stressor (preparation for an expected public speech) was applied at three different time points (and compared with no-stress controls); prior to stimulus presentation and initial learning, immediately after stimulus presentation/learning, and just before memory testing 48 hours later. Both verbal and visual memory retention was measured using a film stimulus. Specifically, it was hypothesized that stress would exert a facilitative effect on encoding and consolidation processes and a detrimental effect on retrieval. While De Quervain and colleagues (2000) have used a similar paradigm using glucocorticoid administration as the manipulation, this study was the first to do so employing a psychological stressor to investigate the effects of stress and endogeneously-released cortisol on each memory phase in a human sample.

Beckner, V.E., Tucker, D.M., Delville, Y., & Mohr, D.C. (2006). Stress facilitates consolidation of verbal memory for a film but does not affect retrieval. Behavioural Neuroscience, 120, 518-527.

de Quervain, D.J., Roozendaal, B., Nitsch, R.M., McGaugh, J.L., & Hock C. (2000). Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 3, 313-314.

[Page vii]

The purpose of the current study was to parse the effects of an acute psychosocial stressor on these separate memory processes by varying the timing of the stressor.

[Page 103]

The psychosocial stressor (preparation for an expected public speech) was applied at 3 different time points (and compared with no-stress controls): prior to stimulus presentation and initial learning, immediately after stimuli presentation/learning, and just before memory testing 48 hours later. Specifically, it was hypothesized that stress would have a facilitative effect on encoding and consolidation processes and a detrimental effect on retrieval. While De Quervain and colleagues (2000) have used a similar paradigm using glucocorticoid administration as the manipulation, this study is the first to do so using a psychological stressor to investigate the effects of stress and endogeneously-released cortisol on each memory phase in a human sample.


De Quervain, D. J., Roozendaal, B., Nitsch, R. M., McGaugh, J. L., & Hock, C. (2000). Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 3, 313-314.

Anmerkungen

Mostly taken verbatim without the source being named.

Interestingly one cannot find the parallel text in the publication Beckner et al. (2006), which is mentioned by the author.

Sichter
(Graf Isolan), Hindemith

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Hypothalamic Pituitary Adrenal Axis

The slower hormonal system to be activated during the stress response is the hypothalamicpituitary-adrenal axis (HPA; Figure 1.5). Unlike the sympathetic-adrenal medulla system (SAMS), which instantly initiates an autonomic response via direct neural stimulation of organs (followed and reinforced by epinephrine release), the HPA stress response relies exclusively on the relatively slower action of adrenal hormones to exert their effect (Sapolsky, 1998). HPA activity thus maintains and builds upon the sympathetic response. Firstly, the paraventricular nucleus of the hypothalamus releases corticotropin releasing factor (CRF), which in turn stimulates the pituitary to release adrenocorticotropin hormone, or ACTH into the bloodstream (for review, see Lovallo & Thomas, 2000; Sapolsky, Romero & Munck, 2000). ACTH makes its way to the adrenal glands, causing the adrenal cortex to release adrenocortical hormones, which are steroids (i.e., lipids derived from cholesterol). There are three classes of hormones produced and released from the adrenal cortex; mineralocorticoids (which help to maintain electrolyte balance), sex hormones, and glucocorticoids (the most important of these in humans is cortisol, while in rodents it is corticosterone; Sherwood, 1997).


Lovallo, W.R. & Thomas, T.L. (2000). In: Cacioppo, J.T., Tassinary & L.G., Berntson, G. (Eds.), Handbook of Psychophysiology (pp. 342–367). New York: Cambridge University Press.

Sherwood, L. (1997). Human Physiology: from Cells to Systems. Belmont, CA: Wadsworth Publishing Company.

Sapolsky (1998). Why zebras don’t get ulcers. New York: W.H. Freeman and Company.

Sapolsky, R.L., Romero, M., & Munck, A.U. (2000). How Do Glucocorticoids Influence Stress Responses? Integrating Permissive, Suppressive, Stimulatory, and Preparative Actions. Endocrine Reviews, 21, 55–89.

HPA

The second hormonal system to be activated during the stress response is the Hypothalamus-Pituary-Adrenal cortex (HPA) axis. Unlike the SAMS, which instantly initiates an autonomic response via direct neural stimulation of organs (followed and reinforced by epinephrine release), the HPA stress response relies exclusively on the relatively slower action of adrenal hormones to exert their effect (Sapolsky, 1998). HPA activity thus maintains and builds upon the sympathetic response. The hypothalamus first releases Corticotropin Releasing Factor (CRF), which in turn stimulates the pituitary to release Adrenocorticotropin Hormone, or ACTH into the bloodstream. ACTH makes its way to the adrenal glands, causing the adrenal cortex to release adrenocortical hormones, which are steroids (lipids derived from cholesterol). There are three classes of hormones produced and released from the adrenal cortex: mineralocorticoids (which help to maintain electrolyte balance), sex hormones, and glucocorticoids (the most important of these in humans is cortisol, while in rodents it is corticosterone) (Sherwood, 1997).


Sapolsky (1998). Why zebras don’t get ulcers. New York: W. H. Freeman and Company.

Sherwood, L. (1997). Human Physiology: From Cells to Systems. Belmont, CA: Wadsworth Publishing Company.

Anmerkungen

Taken nearly verbatim without the source being named.

Sichter
(Graf Isolan), Hindemith

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1.3.2 The Physiology of the Stress Response

Although stressors vary widely, the physiological response is relatively nonspecific. [...] Initiated by the brain and largely mediated by stress hormones, stress-induced changes include an increase in oxygen intake, redirection of blood flow to the muscles, an increase in blood sugar levels to provide the organism with energy, and a behavioral urgency to act in response to a perceived threat (i.e., ‘fight or flight’). Given that all of these activities involve expending energy, there must be conservation elsewhere in the body. Thus digestion, tissue repair and growth, reproductive activities, and immune function are all inhibited by the stress response (Sapolsky, 1998). The stress response also acts on the brain to presumably affect certain cognitive operations and predispose certain types of behavior. Thus in order to understand the effects of stress upon cognition, it is pertinent to understand the physiological stress response.


Sapolsky (1998). Why zebras don’t get ulcers. New York: W.H. Freeman and Company.

2. The Physiology of Stress

Although stressors vary widely, the physiological response is relatively nonspecific. [...] Initiated by the brain and largely mediated by stress hormones, these changes include an increase in oxygen intake, redirecting blood flow to favor the muscles, an increase in blood sugar levels to provide the organism energy, and a behavioral urgency to act (flee, practice, argue, fight). Because all of these activities involve expending energy, there must be conservation elsewhere in the body. Thus digestion, tissue repair and growth, reproductive activities, and immune function are all inhibited by the stress response (Sapolsky, 1998). The stress response also acts on the brain to presumably affect certain cognitive operations and predispose certain types of behavior. Thus to understand the effects of stress on cognition, it is critical to understand the physiological stress response.


Sapolsky (1998). Why zebras don’t get ulcers. New York: W. H. Freeman and Company.

Anmerkungen

Mostly taken verbatim without the source being named.

Sichter
(Graf Isolan), Hindemith

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Retrieval cues can match both intentionally and incidentally encoded information, and each matching feature increases the summed global activation score for the set of items in memory. Retrieval cues can match both intentionally and incidentally encoded information, and each matching feature increases the summed global activation score for the set of items in memory.
Anmerkungen

No reference to the source.

Sichter
(Hindemith) Agrippina1

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In response, Murnane, Phelps and Malmberg (1999) proposed a theory of cueing effects that assumes that there are three general types of information that can match between encoding and retrieval: Item information, Context information, and Ensemble information (thus, it is called the ICE theory). Item information refers to features that received focal processing at encoding (e.g., the conceptual features of the studied words). Context information refers to incidentally-processed features that are bound in a memory trace although they are not central to the memory task at hand. This type of information is also known as associated context. Ensemble information refers to contextual features that are meaningfully integrated with the item information. According to the ICE model, when associated context information is provided in a test cue, the relevant contextual feature is activated across an entire set of items in memory. However, providing integrated context information at retrieval activates contextual features that are uniquely associated with a single item in memory. Murnane, Phelps, & Malmberg (1999) have proposed a theory of cueing effects that assumes that there are three general types of information that can match between encoding and retrieval: Item information, Context information, and Ensemble information (thus, it is called the ICE theory). Item information refers to features that received focal processing at encoding (e.g., the conceptual features of the studied words). Context information refers to incidentally processed features that are bound in a memory trace although they are not

[page 28]

central to the memory task at hand; this type of information is also known as associated context. Ensemble information refers to contextual features that are meaningfully integrated with the item information. According to the ICE model, when associated context information is provided in a test cue, the relevant contextual feature is activated across an entire set of items in memory. However, providing integrated context information at retrieval activates contextual features that are uniquely associated with a single item in memory.

Anmerkungen

The reference to the source is missing.

Sichter
(Hindemith) Agrippina1

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The association between viewed items and the context in which they appear has been termed contextual binding (Chalfonte & Johnson, 1996; Mitchell et al., 2000). The capacity [to encode such associations can be distinguished from the ability to separately encode either the item or its context.] The association between viewed items and the context in which they appear has been termed “contextual binding” (Chalfonte and Johnson, 1996; Mitchell et al., 2000). The capacity to encode such associations can be distinguished from the ability to separately encode either the item or its context.
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[101.] Jm/Fragment 042 11 - Diskussion
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In a more recent study, Smeets and colleagues (2008), found that memory is differentially affected by stress-induced cortisol elevations and sympathetic activity at consolidation and retrieval. Participants were first exposed to a cold pressor task stressor before encoding, during consolidation, before retrieval, or were not stressed and were subsequently subjected to neutral and emotional versions of the DRM word list learning paradigm. Twenty-four hours later, recall of presented words (true recall) and non-presented critical lure words (false recall) was assessed. Results indicated that stress exposure resulted in superior true memory performance in the consolidation stress group and reduced true memory performance in the retrieval stress group compared to the other groups, predominantly for emotional words. These memory-enhancing and memory-impairing effects were strongly related to stress-induced cortisol and sympathetic activity measured via salivary alpha-amylase levels. Neutral and emotional false recall, on the other hand, was neither affected by stress exposure, nor related to cortisol and sympathetic activity following stress. These results demonstrate the importance of stress-induced hormone-related activity in enhancing memory consolidation and in impairing memory retrieval, in particular for emotional memory material. Participants (N=90) were exposed to a stressor before encoding, during consolidation, before retrieval, or were not stressed and then were subjected to neutral and emotional versions of the Deese-Roediger-McDermott word list learning paradigm. Twenty-four hours later, recall of presented words (true recall) and non-presented critical lure words (false recall) was assessed. Results show that stress exposure resulted in superior true memory performance in the consolidation stress group and reduced true memory performance in the retrieval stress group compared to the other groups, predominantly for emotional words. These memory-enhancing and memory-impairing effects were strongly related to stress-induced cortisol and sympathetic activity measured via salivary alpha-amylase levels. Neutral and emotional false recall, on the other hand, was neither affected by stress exposure, nor related to cortisol and sympathetic activity following stress. These results demonstrate the importance of stress-induced hormone-related activity in enhancing memory consolidation and in impairing memory retrieval, in particular for emotional memory material.
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While it is clear to the reader that here the study of Smeets et al. (2008) is presented, it is not clear that simply a large part of the abstract has been copied into the thesis, including the critical interpretation of the study: "These results demonstrate the importance of ..."

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[102.] Jm/Fragment 092 01 - Diskussion
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Rosenberg (1965) scored his 10-question scale that was presented with four response choices, ranging from “strongly agree” to “strongly disagree” as a six-item Guttman scale. The first item included questions 1 through 3 and were denoted a positive score if two or three of its questions were answered positively. Questions 4 and 5 and questions 9 and 10 were aggregated into two other items that were scored positively, if both questions in the item had positive answers. Questions 6 through 8, counted individually, formed the final three items. For the negatively worded RSE questions, responses that expressed disagreement and, hence, were consistent with high self-esteem, were considered positive. Rosenberg (1965) scored his 10-question scale that was presented with four response choices, ranging from •strongly agree• to strongly disagree,• as a six-item Guttman scale. The first item included questions 1 through 3 and received a positive score if two or three of its questions were answered positively. Questions 4 and 5 and questions 9 and 10 were aggregated into two other items that were scored positively, if both questions in the item had positive answers. Questions 6 through 8 counted individually formed the final three items. For the negatively worded RSE questions, responses that expressed disagreement and, hence, were consistent with high self-esteem, were considered positive or •endorsed.•
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[103.] Jm/Fragment 341 14 - Diskussion
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Furthermore, it is widely acknowledged that the hippocampal and PHC regions are responsible for the association of objects with their spatial location in the stimulus environment. Other neuroimaging evidence indicates that these regions are also involved in relational processing, that is, in integrating or binding disparate elements in a complex scene to form a meaningful representation. For example, greater activation of the HF and PHC region occurs when stimulus elements are encoded relationally or bound together rather than encoded individually (Henke et al., 1997, 1999). Thus far, in vivo demonstrations of HF and PHC activations during binding operations have used paradigms that required effortful encoding (Henke et al., 1997, 1999; Montaldi et al., 1998). However, behavioral data suggest that these processes operate without explicit intention. The hippocampal and parahippocampal regions have been shown to be responsible for the association of objects with their spatial location in the stimulus environment (Burgess et al., 2002). Other neuroimaging evidence indicates that these regions are also involved in relational processing (Cohen et al., 1999), that is, in integrating or binding disparate elements in a complex scene to form a meaningful representation. For example, greater activation of the hippocampus and parahippocampal region occurs when stimulus elements are encoded relationally or “bound” together rather than encoded individually (Henke et al., 1997, 1999). Thus far, in vivo demonstration of hippocampal and parahippocampal activations during binding operations have used paradigms that required effortful encoding (Henke et al., 1997, 1999; Montaldi et al., 1998). However, behavioral data suggest that these processes operate without explicit intention (Luck and Vogel, 1997; Cohen et al., 1999).
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Note that the same text has been used also on pages 109, 110 of the thesis: Jm/Fragment 109 21, Jm/Fragment 110 01

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[104.] Jm/Fragment 110 01 - Diskussion
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[For] example, greater activation of the HF and PHC region occurs when stimulus elements are encoded relationally or bound together rather than encoded individually (Henke et al., 1997, 1999). Thus far, in vivo demonstrations of HF and PHC activations during binding operations have used paradigms that required effortful encoding (Henke et al., 1997, 1999; Montaldi et al., 1998). However, behavioral data suggest that these processes operate without explicit intention (Luck & Vogel, 1997; Cohen et al., 1999). In line with Goh and associates (2004)who demonstrated the engagement of MTL areas in contextual binding without explicit task instructions to relate picture elements, we sought to identify behavioural correlates of contextual binding without explicit instruction to do so, in an episodic hippocampallymediated visual paired-associates task For example, greater activation of the hippocampus and parahippocampal region occurs when stimulus elements are encoded relationally or “bound” together rather than encoded individually (Henke et al., 1997, 1999). Thus far, in vivo demonstration of hippocampal and parahippocampal activations during binding operations have used paradigms that required effortful encoding (Henke et al., 1997, 1999; Montaldi et al., 1998). However, behavioral data suggest that these processes operate without explicit intention (Luck and Vogel, 1997; Cohen et al., 1999). In the present study, we sought to identify regions engaged in contextual binding without explicit instruction to do so.
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[105.] Jm/Fragment 109 21 - Diskussion
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Further, the hippocampal and PHC regions have been shown to be responsible for the association of objects with their spatial location in the stimulus environment (Burgess et al., 2002). Other neuroimaging evidence indicates that these regions are also involved in relational processing (Cohen et al., 1999), that is, in integrating or binding disparate elements in a complex scene to form a meaningful representation. The hippocampal and parahippocampal regions have been shown to be responsible for the association of objects with their spatial location in the stimulus environment (Burgess et al., 2002). Other neuroimaging evidence indicates that these regions are also involved in relational processing (Cohen et al., 1999), that is, in integrating or binding disparate elements in a complex scene to form a meaningful representation.
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[106.] Jm/Fragment 072 13 - Diskussion
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However, and importantly in terms of present concerns, the major stumbling block encountered with the use of ERPs is the relatively poor spatial resolution it affords both Experimenters and clinicians. Electrical fields are significantly distorted by skull and scalp tissue, such that the pattern of activity recorded on the scalp may bear little resemblance to the regions of cortex responsible for such activity. As such, it is difficult to ascertain with convincing accuracy whether a potential recorded by a dorsolateral prefrontal electrode actually emanated from the dorsolateral prefrontal cortex. PET and fMRI allow for very high spatial resolution, given that the anatomical structures receiving increased blood flow can be represented in three dimensions. Also, because they do not rely on mere scalp recordings, activity in deep sub-cortical regions may also be observed. This disadvantage limits the use of ERPs in Experimental study, and many laboratories have conducted much research on methods to overcome this apparent deficit. The major stumbling block encountered in the use of ERPs is the relatively poor spatial resolution it affords both experimenters and clinicians. Electrical fields are significantly distorted by skull and scalp tissue, so the pattern of activity recorded on the scalp may bear little resemblance to the regions of cortex responsible for such activity. As such, it is difficult to assert that a potential recorded by a dorsolateral prefrontal electrode emanated from the dorsolateral prefrontal cortex. PET and fMRI allow for very high spatial resolution, because the anatomical structures receiving increased blood flow can be represented in three dimensions. Also, because they do not rely on mere scalp recordings, activity in deep sub-cortical regions may also be seen. This disadvantage limits the use of ERPs in experimental study, and many laboratories have conducted much research on methods to overcome this apparent deficit.
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[107.] Jm/Fragment 071 01 - Diskussion
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The time-course of processing in the cortex may be seen with millisecond accuracy. In this particular facet of functional brain activity recording, ERPs are considerably superior to the other major techniques available such as Positron Emission Tomography (PET) and functional Magnetic Resonance Imaging (fMRI). Both of these imaging techniques are constructed upon the concept that increased cognitive processing in an area of cortex requires increased regional cerebral blood flow (rCBF) to support the local energetic demands of the tissue for nutrients and oxygen. There is a significant time-lag involved in such approaches, due to the relatively slow speed at which blood flows through the brain (in comparison to electrical impulses). Also, a blocked design must be used in most imaging studies, such that a real-time record of processing cannot be obtained. The time-course of processing in the cortex

[page 6]

may be seen with millisecond accuracy. In this facet of functional brain activity recording, ERPs is considerably superior to the other major options available, Positron Emission Tomography (PET) and functional Magnetic Resonance Imaging (fMRI). Both of these imaging techniques rely on the idea that increased cognitive processing in an area of cortex requires increased regional cerebral blood flow (rCBF) to support the local energetic demands of the tissue for nutrients and oxygen. There is a significant time-lag involved in such approaches, due to the relatively slow speed at which blood flows through the brain (in comparison to electrical impulses). Also, a blocked design must be used in most imaging studies, so a real-time record of processing cannot be obtained.

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[108.] Jm/Fragment 062 20 - Diskussion
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In 1939, Davis published a paper in which he extracted the changes in EEG due to a sensory stimulus, naming it an Evoked Potential (EP). Renshaw, Forbes and Morison proposed the possible relationship between the slow potentials of neurons and the oscillations of the EEG in 1940, leading to the foundation of the American EEG Society. Up until the 1950s there was no set method of electrode placement on the scalp, leading to a committee headed by Jasper developing the international 10-20 placement system. A year later, Davis (1939) published a paper in which he extracted the changes in EEG due to a sensory stimulus, naming it an Evoked Potential (EP). Renshaw, Forbes and Morison proposed the possible relationship between the slow potentials of neurons and the oscillations of the EEG in 1940, leading to the foundation of the American EEG Society. Up until the 1950s there was no set method of electrode placement on the scalp, leading to a committee headed by Jasper developing the international 10-20 placement system.
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Continuation here: Jm/Fragment_063_01

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[109.] Jm/Fragment 070 22 - Diskussion
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Given that electrical potentials travel through both the bone and skin of the skull and scalp at high speed leading to almost instantaneous recording of the electrical activity of the brain, ERPs provide very [high temporal resolution.] Electrical potentials travel through the bone and skin of the skull and scalp at high speed leading to almost instantaneous recording of the electrical activity of the brain, thus providing very high temporal resolution.
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[110.] Jm/Fragment 070 01 - Diskussion
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It has been repeatedly demonstrated by correlating scalp-recorded EEG with intracranial neuronal discharges in the monkey and the cat, that the polarity of ERPs, are related to either excitation or inhibition of cells. Comparison of evoked potentials and neuronal spiking activity reveals that neuronal discharges/firing in thalamocortical cells seem to result in negative ERP components, while cellular inhibition underlies positive potentials. Thus EPSPs/depolarisations appear responsible for negative ERP deflections, while IPSPs/hyperpolarisations are the cause of scalp-recorded positivities. Specifically, the scalp recorded negative shifts seem to be due to the depolarisation of pyramidal cell dendrites, which results in an extracellular surface current sink, with the opposite situation the case for scalp recorded positives. The relationship between neuronal activity and scalp-recorded potentials is shown in Figures 2.5 and 2.6 above, from Coenen (1995). Although this polarity reversal between intracranial and scalp recorded activity is true in most cases, the opposite relationship, where scalp positives are due to neuronal excitation and negatives to inhibition, has also been found on occasion. It has been repeatedly demonstrated by correlating scalp recorded EEG with intracranial neuronal discharges in the monkey and the cat that the polarity of ERPs are related to either excitation or inhibition of cells. Comparison of evoked potentials and neuronal spiking activity reveals that neuronal discharges/firing in thalamocortical cells seem to result in negative ERP components, while cellular inhibition underlies positive potentials. Thus EPSPs/depolarisations appear responsible for negative ERP deflections, while IPSPs/hyperpolarisations are the cause of scalp-recorded positivities. Specifically, the scalp recorded negative shifts seem to be due to the depolarisation of pyramidal cell dendrites, which results in an extracellular surface current sink, with the opposite situation the case for scalp recorded positives. The relationship between neuronal activity and scalp-recorded potentials is shown in Figures 3 and 4, from Coenen (1995). Although this polarity reversal between intracranial and scalp recorded activity is true in most cases, the opposite relationship, where scalp positives are due to neuronal excitation and negatives to inhibition, has also been found on occasion.
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2.3.3 Physiological basis of ERPs

2.3.3.1 Electrical activity in the brain

Communication in the central nervous system takes place through the transmission of electrochemical signals between nerve cells, or neurons (see Figure 2.2). Messages to either excite or inhibit activity in other neurons are passed via the release of neurotransmitter substances from the axon of the efferent (or pre-synaptic) cell to the dendritic tree or cell body of the afferent (or post-synaptic) neuron. The neurotransmitters influence the activity of the neuron by binding to receptors which alter the electrical potential across the membrane of the cell. Due to the constant influx and outflow of both positively and negatively charged ions across this membrane, the equilibrium state, or resting potential, of a neuron is approximately –70 mV. Any deviation from this state will make the cell either more or less likely to generate an action potential. An excitatory signal from a presynaptic cell will cause certain ion channels to open or close, with the result that the membrane potential rises from – 70 mV to 0 mV and possibly higher. Such excitatory impulses are termed Excitatory Post- Synaptic Potentials (EPSPs). If the membrane potential rises above a particular threshold level, approximately +30 mV, then an action potential is generated in the neuron, and [neurotransmitter is released onto another cell.]

Physiological basis of ERPs

Communication in the central nervous system takes place through the transmission of electrochemical signals between nerve cells, or neurons (see Figure 2). Messages to either excite or inhibit activity in other neurons are passed via the release of neurotransmitter substances from the axon of the efferent (or pre-synaptic) cell to the dendritic tree or cell body of the afferent (or post-synaptic) neuron.

The neurotransmitters influence the activity of the neuron by binding to receptors which alter the electrical potential across the membrane of the cell. Due to the constant influx and outflow of both positively and negatively charged ions across this membrane, the equilibrium state, or resting potential, of a neuron is approximately –70 mV. Any deviation from this state will make the cell either more or less likely to generate an action potential. An excitatory signal from a presynaptic cell will cause certain ion channels to open or close, with the result that the membrane potential rises from –70 mV to 0 mV and possibly higher. Such excitatory impulses are termed Excitatory Post-Synaptic Potentials (EPSPs). If the membrane potential rises above a particular threshold level, approximately +30 mV, then an action potential is generated in the neuron, and neurotransmitter is released onto another cell.

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Neural Current Sources originate at the cell membrane and represent a deviation from the equilibrium state or resting potential. During an EPSP, a local current sink is produced, which draws positive ions into the cell, thereby moving the potential closer to 0 mV. A sink may be thought of as a negative source. Local sinks are balanced by distant passive sources; as the sink draws ions into the cell, thus depolarising the membrane, these ions move through the neuron and are ejected at some other location, known as a (positive) source. For example, if a sink existed at a branch of the cell’s dentritic tree, the distant source might occur at the cell body, or near the axon hillock. The co-occurrence of the positive source at one location, and the negative sink at another, means that the cell may effectively be viewed as a dipole. In an IPSP, the opposite situation occurs. A local source is produced, which emits positive ions, thereby lowering the membrane potential. This source is balanced by a distant sink, which takes in ions at another location on the cell. Again, this may be considered as a dipole. The EEG gives a macroscopic view of the activity of these sinks and sources. Neural Current Sources originate at the cell membrane and represent a deviation from the equilibrium state or resting potential. During an EPSP, a local current sink is produced, which sucks positive ions into the cell, thereby moving the potential closer to 0 mV. A sink may be thought of as a negative source. Local sinks are balanced by distant passive sources; as the sink draws ions into the cell, thus depolarising the membrane, these ions move through the neuron and are ejected at some other location, known as a (positive) source. For example, if a sink existed at a branch of the cell’s dentritic tree, the distant source might occur at the cell body, or near the axon hillock. The co-occurrence of the positive source at one location and the negative sink at another means that the cell may effectively be viewed as a dipole.

In an IPSP, the opposite situation occurs. A local source is produced, which emits positive ions, thereby lowering the membrane potential. This source is balanced by a distant sink, which takes in ions at another location on the cell. Again, this may be considered as a dipole. The EEG gives a macroscopic view of the activity of these sinks and sources.

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[Although we] can only provide a brief overview here, a detailed account of the workings of this technique is provided by Nunez (1990).

EEG and ERPs record from the scalp the electrical activity (produced by sinks and sources) of populations of pyramidal cells which form the grey matter of the cortical surface. If a scalp potential records activity due to current sources over an area of less than 1 cm², then the large number of sources may be considered as a single dipole source. Usually, however, scalp potentials are due to larger areas of activity. When a large number of dipoles fire with synchronous activity, and their polarities are the same (i.e. all their positive terminals or sources are adjacent to other positives), as can happen with the densely interconnected pyramidal neurons of the cortical surface, then the group could be considered to form a homogenous dipole layer. However, dipole layers rarely occur with completely homogenous polarities of sinks and sources. The more common occurrence is for the layer to consist of a mixture of polarities of dipoles, in which case the overall potential will reflect the majority of dipole polarities.

Although we can only provide a brief overview here, a detailed account of the workings of this technique is provided by Nunez (1990).

EEG and ERPs record from the scalp the electrical activity (produced by sinks and sources) of populations of pyramidal cells which form the grey matter of the cortical surface. If a scalp potential recorded activity due to current sources over an area of less than 1 cm², then the large number of sources may be considered as a single dipole source. Usually, however, scalp potentials are due to larger areas of activity. When a large number of dipoles fire with synchronous activity, and their polarities are the same (i.e. all their positive terminals or sources are adjacent to other positives), as can happen with the densely interconnected pyramidal neurons of the cortical surface, then the group could be considered to form a homogenous dipole layer. However, dipole layers rarely occur with completely homogenous polarities of sinks and sources. The more common occurrence is for the layer to consist of a mixture of polarities of dipoles, in which case the overall potential will reflect the majority of dipole polarities.

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The rise in membrane potential due to an EPSP is called depolarisation. In contrast, Inhibitory Post-Synaptic Potentials (IPSPs) render cell firing less likely by lowering the membrane potential, thereby pushing it further from the threshold level for action potential propagation. This lowering of the potential across the membrane is called hyperpolarisation. It is the summated effects of these depolarisations and hyperpolarisations (which may collectively be termed Neural Current Sources), rather than the action potentials themselves, that are recorded by EEG and ERPs. The rise in membrane potential due to an EPSP is called depolarisation.

In contrast, Inhibitory Post-Synaptic Potentials (IPSPs) make cell firing less likely by lowering the membrane potential, thereby pushing it further from the threshold level for action potential propagation. This lowering of the potential across the membrane is called hyperpolarisation. It is the summated effects of these depolarisations and hyperpolarisations (which may collectively be termed Neural Current Sources), rather than the action potentials themselves, that are recorded by EEG and ERPs.

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Placing EEG in a historical context, Caton (1875) described the first sensory evoked electrical responses from the surface of the brains of rabbits and monkeys using single electrode recording. Beck (1890) furthered the work of Caton by studying the electrical brain responses of rabbits and dogs to presentation of sensory stimuli. Within 40 years, recordings of electrical brain potentials had moved from animals to humans, and in 1929, Hans Berger published the first recorded study of scalp recordings of human EEGs in which he measured the electrical activity of the human brain by placing an electrode on the scalp, amplifying the signal, and plotting the changes in voltage over time. Caton (1875) described the first sensory evoked electrical responses from the surface of the brains of rabbits and monkeys using single electrode recording. Beck (1890) furthered the work of Caton by studying the electrical brain responses of rabbits and dogs to presentation of sensory stimuli. Within 40 years, recordings of electrical brain potentials had moved from animals to humans, and in 1938 Hans Berger published the first recorded study of scalp recordings of human EEGs, in which he first used the term “Elektrenkephalogramm”.
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The year 1929 seems to be correct: Wikipedia

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(Hindemith) Agrippina1

[116.] Jm/Fragment 063 01 - Diskussion
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[Dawson] (1954) extended the EP extraction techniques introduced by Davis (1939), by averaging large numbers of EPs to increase signal-to-noise ratio thereby reducing the amount of conflicting data being recorded for each response. [...] By the 1970s, ERPs were being widely applied in clinical diagnosis, [...] Dawson (1954) extended the EP extraction techniques introduced by Davis (1939), by averaging large numbers of EPs to increase signal-to-noise ratio, beginning the study of Event Related Potentials (ERPs). By the 1970s, ERPs were being widely applied in clinical diagnosis.
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(Hindemith) Agrippina1

[117.] Jm/Fragment 064 01 - Diskussion
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[These wave-forms are measured as the difference between the electrical activity of a baseline reference electrode attached to an electrically inactive site, such as the mastoid bone below the ear or the naison] on the nose, and the electrical activity of the areas of the brain covered by the electrodes. These changes allow neuroscientists to determine what areas of brain are being stimulated at a given time (and therefore which brain areas are involved in a given process), precisely when these areas become activated and what happens in these areas when people make an error. These wave-forms are measured as the difference between the electrical activity of a baseline reference electrode attached to an electrically inactive site, such as the mastoid bone below the ear or the naison on the nose, and the electrical activity of the areas of the brain covered by the electrodes. These changes allow neuroscientists to determine what areas of brain are being stimulated at a given time (and therefore which brain areas are involved in a given process), precisely when these areas become activated and what happens in these areas when people make an error.
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The copied text starts already on the previous page: Jm/Fragment 063 18

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(Hindemith) Agrippina1

[118.] Jm/Fragment 063 18 - Diskussion
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2.3.2 Event-Related Potentials (ERPs)

More specifically for present purposes, ERPs are changes in the ongoing electrical activity of the brain (electroencephalogram, or EEG) which are caused by the specific occurrence of a cognitive, motor or perceptual event. Any changes in EEG due to the demands of the task are amplified, averaged and extracted as ERP waveforms (see Figure 2.1). These wave-forms are measured as the difference between the electrical activity of a baseline reference electrode attached to an electrically inactive site, such as the mastoid bone below the ear or the naison [on the nose, and the electrical activity of the areas of the brain covered by the electrodes.]

Event-Related Potentials (ERPs) are changes in the ongoing electrical activity of the brain (Electroencephalograms, or EEGs) which are caused by the specific occurrence of a cognitive, motor or perceptual event. Any changes in EEG due to the demands of the task are amplified, averaged and extracted as ERP waveforms (see Figure 1). These wave-forms are measured as the difference between the electrical activity of a baseline reference electrode attached to an electrically inactive site, such as the mastoid bone below the ear or the naison on the nose, and the electrical activity of the areas of the brain covered by the electrodes.
Anmerkungen

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Note that there exists no figure 2.1. in the thesis.

The copied text continues on the next page: Jm/Fragment 064 01

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(Hindemith) Agrippina1

[119.] Jm/Fragment 029 17 - Diskussion
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Exposure to highly stressful events is known to trigger a variety of physiological reactions, of which many are related to the activation of stress-responsive sympatho adrenal-medullary (SAM) and hypothalamic–pituitary–adrenal (HPA) axes. A plethora of research has revealed that secretion of glucocorticoids (GCs) in response to HPA axis stimulation may modulate memory functioning (e.g., de Kloet et al., 1999; McGaugh, 2000; Roozendaal, 2000). However, the precise direction of stress-induced GC effects on memory performance is far from succinct. Animal studies, for example, have shown that GCs can exert both facilitating (e.g., on aversive conditioning) as well as impairing effects on memory (e.g., de Kloet et al., 1999; Lupien & McEwen, 1997; McGaugh & Roozendaal, 2002). Most people are familiar with highly stressful events. Exposure to such events is known to trigger a variety of physiological reactions, of which many are related to the activation of stress-responsive sympathoadrenal medullary (SAM) and hypothalamic–pituitary–adrenal (HPA) axes. A plethora of research has revealed that secretion of glucocorticoids (GCs) due to HPA axis stimulation may modulate memory functioning (e.g., de Kloet et al., 1999; McGaugh, 2000; Roozendaal, 2000). However, the precise direction of stress-induced GC effects on memory performance is far from clear. Animal studies, for example, have shown that GCs can have facilitating (e.g., on aversive conditioning), but also impairing effects on memory (e.g., de Kloet et al., 1999; Lupien and McEwen, 1997; McGaugh and Roozendaal, 2002).
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(Hindemith) Agrippina1

[120.] Jm/Fragment 030 01 - Diskussion
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[Similarly,] studies employing human participants have reported that acute GC administration may enhance or disrupt memory, yet the precise conditions under which these effects occur are thus far ill-understood (for reviews, see Het et al., 2005; Lupien et al., 2005; Lupien & Lepage, 2001; Wolf, 2003). Similarly, studies relying on human participants have reported that acute GC administration may enhance or disrupt memory, yet the precise conditions under which these effects occur are ill-understood (for reviews, see Het et al., 2005; Lupien et al., 2005; Lupien and Lepage, 2001; Wolf, 2003).
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The copies text starts already on the previous page: Jm/Fragment_029_17

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[121.] Jm/Fragment 274 14 - Diskussion
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We herein demonstrate that the modification of episodic memories depends critically upon their preceding reactivation as suggested by the reconsolidation account. Similar to what has been found for Pavlovian conditioning (e.g., Nader et al., 2000), instrumental conditioning (e.g., Wang et al., 2005), and human procedural memory (Walker et al., 2003), reactivated episodic memories also undergo a time-dependent reconsolidation process: incorporation of new information did not occur immediately but was seen 24 hours after memory reactivation and subsequent presentation of new material. We show that the modification of episodic memories depends critically upon their preceding reactivation as suggested by the reconsolidation account.

Similar to what has been found for Pavlovian conditioning (e.g., Nader et al. 2000), instrumental conditioning (e.g., Wang et al. 2005), and human procedural memory (Walker et al. 2003), reactivated episodic memories also undergo a time-dependent reconsolidation process: Incorporation of new information did not occur immediately but was seen two days after memory reactivation and subsequent presentation of new material.

Anmerkungen

The source of the copied text is not referenced, although the source seems to have shown the same phenomenon.

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(Hindemith) Agrippina1

[122.] Jm/Fragment 286 21 - Diskussion
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Memories for hippocampus-dependent tasks undergo reconsolidation (Mactutus et al., 1979; Przybyslawski, Roullet & Sara, 1999; Schneider & Sherman, 1968). For example, using a radial arm maze with rats, systemic postreactivation injections of propranol were [effective at producing amnesia if the memory was first reactivated (Przybyslawski et al., 1999).] Results from previous studies have suggested that memories for hippocampus-dependent tasks can undergo reconsolidation (Mactutus et al., 1979; Przybyslawski et al., 1999; Schneider and Sherman, 1968). For example, using a radial arm maze, systemic postreactivation injections of propranol were effective at producing amnesia if the memory was first reactivated (Przybyslawski et al., 1999).
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The copied text continues on the next page: Jm/Fragment 287 01

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(Hindemith) Agrippina1

[123.] Jm/Fragment 287 13 - Diskussion
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In animal studies, post-retrieval administration of propranolol has been found to disrupt spatial memory and inhibitory avoidance learning in rodents (Przybyslawski et al., 1999), as well as auditory fear conditioning (Debiec & Ledoux, 2004), with both findings explained in terms of impaired reconsolidation processes. Tronel and Alberini (2007) demonstrated that reconsolidation might also be dependent upon the glucocorticoid system, as they found that a glucocorticoid receptor antagonist disrupted conditioned fear in rats after reactivation of an inhibitory avoidance memory. In a similar vein, Maroun and Akirav (2007) found an impairing effect of stress on reconsolidation in rats, which was reversed by a glucocorticoid receptor antagonist. Post-retrieval administration of propranolol has been found to disrupt spatial memory and inhibitory avoidance learning in rodents (Przybyslawski et al., 1999), as well as auditory fear conditioning (Debiec & Ledoux, 2004), and both findings have been explained in terms of impaired reconsolidation processes. Tronel and Alberini (2007) have recently shown that reconsolidation might also be dependent on the glucocorticoid system, as they found that a glucocorticoid receptor antagonist can disrupt conditioned fear in rats after reactivation of an inhibitory avoidance memory. In line with that, Maroun and Akirav (2007) have found an impairing effect of stress on reconsolidation in rats, which was reversed by a glucocorticoid receptor antagonist.
Anmerkungen

The source is not given.

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(Hindemith) Agrippina1

[124.] Jm/Fragment 349 23 - Diskussion
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As such, the modification of episodic memories depends critically upon their preceding reactivation as suggested by the reconsolidation account. Similar to what has been found for Pavlovian conditioning (e.g., [Nader et al., 2000), instrumental conditioning (e.g., Wang et al., 2005), and human procedural memory (Walker et al., 2003), reactivated episodic memories, in our study, underwent similar time-dependent reconsolidation processing.] We show that the modification of episodic memories depends critically upon their preceding reactivation as suggested by the reconsolidation account.

Similar to what has been found for Pavlovian conditioning (e.g., Nader et al. 2000), instrumental conditioning (e.g., Wang et al. 2005), and human procedural memory (Walker et al. 2003), reactivated episodic memories also undergo a time-dependent reconsolidation process:

Anmerkungen

The source is not referenced.

The same passage appears also on page 274 of the thesis: Jm/Fragment 274 14

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(Hindemith) Agrippina1

[125.] Jm/Fragment 038 01 - Diskussion
Bearbeitet: 11. January 2014, 09:40 Hindemith
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[In many of the human studies demonstrating an] impairing effect of elevated cortisol on memory, the stressor or glucocorticoid is applied before stimulus presentation and learning, and recall is tested within 1–2 hours. In such a paradigm, cortisol levels are elevated during all memory phases: the learning period (initial encoding of the information), consolidation (the continuous transfer of information into longer term storage), and retrieval (recall of information from memory stores). Disruption of any one of these memory processes could account for detrimental effects of stress on memory and might also obscure any facilitated process. Roozendaal (2002) has theorized that under stressful conditions, consolidation of novel information related to the situation is enhanced such that one is more likely to later remember information associated with the stressful experience. However, in order to facilitate this new learning during arousing situations, competing processes of retrieving old information (which could result in retroactive interference) may be inhibited. Thus, it may be impaired retrieval that accounts for many of the human findings cited above, rather than stress effects on learning or consolidation.

Indeed, recent studies that have managed to isolate consolidation as a target process point to a facilitative effect of stress. These investigations typically administer the stress induction protocol or corticosteroids prior to or immediately following training (i.e., during encoding and consolidation), followed by retention testing at least 24 hr later. Retrieval is therefore tested after corticosterone levels have returned to baseline, thereby isolating the effect of glucocorticoids on consolidation of new memories. Animal studies using this paradigm have generally found a facilitative effect of moderate levels of glucocorticoids on consolidation (Conrad, Lupien & McEwen, 1999; Oitzl & de Kloet, 1992; Roozendaal & McGaugh, 1996; Sandi, Loscertales & Guaza, 1997). Several recent human studies have also found a facilitative effect of stress or administered cortisol on encoding and consolidation of visual information with affective content when recall is tested at least 24 hr after learning (Buchanan & Lovallo, 2001; Cahill, Gorski & Le, 2003); an additional study found this for [both emotionally arousing and neutral information (Abercrombie et al., 2003).]


Abercrombie, H.C., Kalin, N.H., Thurow, M.E., Rosenkranz, M.A., & Davidson, R.J. (2003). Cortisol variation in humans affects memory for emotionally laden and neutral information. Behavioral Neuroscience, 117, 505-516.

Buchanan, T.W. & Lovallo, W.R. (2001). Enhanced memory for emotional material following stress-level cortisol treatment in humans. Psychoneuroendocrinology, 26, 307–317.

Cahill L, Gorski L, & Le K (2003). Enhanced human memory consolidation with post-learning stress: interaction with the degree of arousal at encoding. Learning and Memory, 10, 270–274.

Conrad, C.D., Lupien, S.J., & McEwen, B.S. (1999). Support for a bimodal role for Type II adrenal steroid receptors in spatial memory. Neurobiology of Learning and Memory, 72, 39-46.

Oitzl, M.S. & de Kloet, E.R. (1992). Selective corticosteroid antagonists modulate specific aspects of spatial orientation learning. Behavioural Neuroscience, 106, 62-71.

Roozendaal, B. (2002). Stress and memory: opposing effects of glucocorticoids on memory consolidation and memory retrieval. Neurobiology of Learning and Memory, 78, 578-595.

Roozendaal, B. & McGaugh, J.L. (1996). Amygdaloid nuclei lesions differentially affect glucocorticoid-induced memory enhancement in an inhibitory avoidance task. Neurobiology of Learning and Memory, 65, 1– 8.

Sandi, C., Loscertales, M., & Guaza, C. (1997). Experience-dependent facilitating effect of corticosterone on spatial memory formation in the water maze. European Journal of Neuroscience, 9, 637–642.

[Page 518]

In many of the human studies demonstrating an impairing effect of elevated cortisol on memory, the stressor or glucocorticoid is applied before stimulus presentation and learning, and recall is tested within 1–2 hr. In such a paradigm, cortisol levels are elevated during all memory phases: the learning period (initial encoding of the information), consolidation (the continuous transfer of information into longer term storage), and retrieval (recall of information from memory stores). Disruption of any one of these memory processes could account for detrimental effects of stress on memory and might also obscure any facilitated process. Roozendaal (2002) has theorized that under stressful conditions, consolidation of novel information related to the situation is enhanced so that one is more likely to later remember where the lion naps or when the hostile supervisor takes his coffee break. However, in order to facilitate this new learning during

[Page 519]

arousing situations, competing processes of retrieving old information (which could result in retroactive interference) may be inhibited. Thus, it may be impaired retrieval that accounts for many of the human findings cited above, rather than stress effects on learning or consolidation.

Indeed, recent studies that have managed to isolate consolidation as a target process point to a facilitative effect of stress. These investigations typically administer the stress induction or corticosteroids prior to or immediately following training (during encoding and consolidation), followed by retention testing at least 24 hr later. Retrieval is therefore tested after corticosterone levels have returned to baseline, thereby isolating the effect of glucocorticoids on consolidation of new memories. Animal studies using this paradigm have generally found a facilitative effect of moderate levels of glucocorticoids on consolidation (Conrad, Lupien, & McEwen, 1999; Oitzl & de Kloet, 1992; Roozendaal & McGaugh, 1996; Sandi, Loscertales, & Guaza, 1997). Several recent human studies have also found a facilitative effect of stress or administered cortisol on encoding and consolidation of visual information with affective content when recall is tested at least 24 hr after learning (Buchanan & Lovallo, 2001; Cahill, Gorski, & Le, 2003); an additional study found this for both emotionally arousing and neutral information (Abercrombie, Kalin, Thurow, Rosenkranz, & Davidson, 2003).


Abercrombie, H. C., Kalin, N. H., Thurow, M. E., Rosenkranz, M. A., & Davidson, R. J. (2003). Cortisol variation in humans affects memory for emotionally laden and neutral information. Behavioral Neuroscience, 117, 505–516.

Buchanan, T. W., & Lovallo, W. R. (2001). Enhanced memory for emotional material following stress-level cortisol treatment in humans. Psychoneuroendocrinology, 26, 307–317.

Cahill, L., Gorski, L., & Le, K. (2003). Enhanced human memory consolidation with post-learning stress: Interaction with the degree of arousal at encoding. Learning & Memory, 10, 270–274.

Conrad, C. D., Lupien, S. J., & McEwen, B. S. (1999). Support for a bimodal role for Type II adrenal steroid receptors in spatial memory. Neurobiology of Learning and Memory, 72, 39–46.

Oitzl, M. S., & de Kloet, E. R. (1992). Selective corticosteroid antagonists modulate specific aspects of spatial orientation learning. Behavioral Neuroscience, 106, 62–71.

Roozendaal, B. (2002). Stress and memory: Opposing effects of glucocorticoids on memory consolidation and memory retrieval. Neurobiology of Learning and Memory, 78, 578–595.

Roozendaal, B., & McGaugh, J. L. (1996). Amygdaloid nuclei lesions differentially affect glucocorticoid-induced memory enhancement in an inhibitory avoidance task. Neurobiology of Learning and Memory, 65, 1–8.

Sandi, C., Loscertales, M., & Guaza, C. (1997). Experience-dependent facilitating effect of corticosterone on spatial memory formation in the water maze. European Journal of Neuroscience, 9, 637–642.

Anmerkungen

Although nearly identical (even with regard to the references) nothing has been marked as a citation. Beckner et al. are mentioned on the previous page, but without indication that the following page will be a copy from their paper.

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