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Autor     Victoria Elizabeth Beckner
Titel    The effects of stress on different stages of memory
Ort    Austin
Datum    August 2004
Anmerkung    PhD thesis University of Texas at Austin
URL    http://repositories.lib.utexas.edu/bitstream/handle/2152/1188/becknerve85191.pdf

Literaturverz.   

no
Fußnoten    no
Fragmente    11


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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.

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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.

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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.

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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.

Anmerkungen

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Nothing has been marked as a citation.

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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.

Anmerkungen

There is no entry for Roozendaal, Quirarte & McGaugh (1997) in the list of references in Jm.

Nothing has been marked as a citation.

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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.

Anmerkungen

Nothing has been marked as a citation.

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(Graf Isolan) Agrippina1

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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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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.

Anmerkungen

The source is not mentioned anywhere in the thesis.

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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

The source is not mentioned anywhere in the thesis.

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

[11.] Jm/Fragment 332 10 - Diskussion
Zuletzt bearbeitet: 2014-01-13 07:35:44 Graf Isolan
Beckner 2004, Fragment, Gesichtet, Jm, SMWFragment, Schutzlevel sysop, Verschleierung

Typus
Verschleierung
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 332, Zeilen: 10-24
Quelle: Beckner 2004
Seite(n): 30, 31, Zeilen: 30: 14ff; 31: 1ff
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.

Anmerkungen

The source is mentioned nowhere in the thesis.

Sichter
(Hindemith) Agrippina1

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