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Psychopharmacology (Berl). 2007 Oct;194(2):261-9. Epub 2007 Jun 24.

Emotion-induced retrograde amnesia varies as a function of noradrenergic-glucocorticoid activity.

Author information

1
Department of Psychiatry, University of Bonn, Sigmund-Freud-Str. 25, 53105, Bonn, Germany. renehurlemann@gmx.de

Abstract

RATIONALE:

Privileged episodic encoding of an aversive event often comes at a cost of neutral events flanking the aversive event, resulting in decreased episodic memory for these neutral events. This peri-emotional amnesia is amygdala-dependent and varies as a function of norepinephrine activity. However, less is known about the amnesiogenic potential of cortisol.

OBJECTIVE:

We used a strategy of pharmacologically potentiating cortisol and norepinephrine activity to probe the putative neurochemical substrates of peri-emotional amnesia.

MATERIALS AND METHODS:

Fifty-four healthy individuals participated in a randomized double-blind placebo-controlled study. Within the experimental context of an established peri-emotional amnesia paradigm, we tested the amnesiogenic potential of hydrocortisone (30 mg p.o.) in the presence or absence of the norepinephrine-reuptake inhibitor reboxetine (4 mg p.o.).

RESULTS:

Under dual challenge conditions, we observed a linear dose-response relationship in the magnitude and duration of emotion-induced retrograde amnesia.

CONCLUSIONS:

Our results are consistent with a phenotypic expression of retrograde amnesia varying as a function of norepinephrine and cortisol coactivation during episodic encoding of aversive events. Our study demonstrates that the adverse cognitive and behavioral sequelae of aversive emotion can be experimentally modeled by a pharmacological manipulation of its putative neurochemical substrates.

PMID:
17588225
PMCID:
PMC2633118
DOI:
10.1007/s00213-007-0836-6
[Indexed for MEDLINE]
Free PMC Article

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