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Reconsolidation: Behavioural and Electrophysiological Sequelae of Context and Stress in Human Episodic Memory

von Dr. Jennifer L. Moore

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[1.] Jm/Fragment 047 01 - Diskussion
Zuletzt bearbeitet: 2014-02-19 00:24:44 Hindemith
BauernOpfer, Fragment, Gesichtet, Jm, Lee 2009, SMWFragment, Schutzlevel sysop

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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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