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Noradrenergic–glucocorticoid mechanisms in emotion-induced amnesia: from adaptation to disease

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Abstract

Discussions

The interaction of emotion and episodic encoding has costs and benefits. These costs and benefits have been characterized in oddball experiments, where a violation of prevailing neutral context through aversive oddballs is associated with subsequent hypermnesia for the aversive oddball and peri-emotional amnesia for the neutral context. Both hypermnesia and peri-emotional amnesia are amygdala-dependent and vary as a function of noradrenergic–glucocorticoid input to the amygdala during emotional episodic encoding. Pharmacological enhancement of this input allows to model the maladaptive effects of emotion on episodic encoding. Extrapolation of these findings to conditions of emotional trauma suggests that disinhibited noradrenergic–glucocorticoid signaling could serve as a crucial etiological contributor to the pathogenesis of peri-traumatic amnesia (PTA) and post-traumatic stress disorder (PTSD).

Conclusions

Immediate pharmacological blockade of noradrenergic–glucocorticoid signaling might prove effective in the secondary prevention of PTA and PTSD.

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Acknowledgment

The author gratefully acknowledges fruitful discussions with and excellent contributions by Raymond J. Dolan (London) and Wolfgang Maier (Bonn). This work was supported by a German Research Foundation (DFG) grant (HU1302/2-1), a German Federal Ministry of Education and Research (BMBF) grant (01GW0671), and a BONFOR fellowship.

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  1. Department of Psychiatry, University of Bonn, Sigmund-Freud-Str. 25, 53105, Bonn, Germany

    René Hurlemann

  2. Brain Imaging Center West, Institute of Medicine, Research Center Juelich, 52425, Juelich, Germany

    René Hurlemann

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Hurlemann, R. Noradrenergic–glucocorticoid mechanisms in emotion-induced amnesia: from adaptation to disease. Psychopharmacology 197, 13–23 (2008). https://doi.org/10.1007/s00213-007-1002-x

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