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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 034 01 - Diskussion
Zuletzt bearbeitet: 2014-01-13 07:28:31 Graf Isolan
Beckner 2004, Fragment, Gesichtet, Jm, SMWFragment, Schutzlevel sysop, Verschleierung

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Graf Isolan
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Untersuchte Arbeit:
Seite: 34, Zeilen: 1-13 (complete)
Quelle: Beckner 2004
Seite(n): 12, Zeilen: 17-28
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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There is no entry for Roozendaal, Quirarte & McGaugh (1997) in the list of references in Jm.

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Sichter
(Graf Isolan), Hindemith


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