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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 035 01 - Diskussion
Zuletzt bearbeitet: 2014-01-12 22:01:40 Graf Isolan
Beckner 2004, Fragment, Gesichtet, Jm, KomplettPlagiat, SMWFragment, Schutzlevel sysop

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Graf Isolan
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Seite: 35, Zeilen: 1ff (complete)
Quelle: Beckner 2004
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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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(Graf Isolan) Agrippina1


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