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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 029 04 - Diskussion
Zuletzt bearbeitet: 2014-02-20 22:22:18 Schumann
Fragment, Gesichtet, Jm, Nadel et al 2002, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 29, Zeilen: 4-13
Quelle: Nadel et al 2002
Seite(n): S4, Zeilen: l.col: 24ff
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.

Anmerkungen

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(Hindemith) Agrippina1

[2.] Jm/Fragment 029 17 - Diskussion
Zuletzt bearbeitet: 2014-01-12 20:50:56 Graf Isolan
Fragment, Gesichtet, Jm, SMWFragment, Schutzlevel sysop, Smeets et al 2007, Verschleierung

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Untersuchte Arbeit:
Seite: 29, Zeilen: 17-25
Quelle: Smeets et al 2007
Seite(n): 116, Zeilen: l.col: 1ff
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).
Anmerkungen

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Sichter
(Hindemith) Agrippina1


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