Chronic Stress Triggers Social Aversion via Glucocorticoid Receptor in Dopaminoceptive Neurons

Author:

Barik Jacques1234,Marti Fabio345,Morel Carole345,Fernandez Sebastian P.346,Lanteri Christophe237,Godeheu Gérard237,Tassin Jean-Pol237,Mombereau Cédric348,Faure Philippe345,Tronche François1234

Affiliation:

1. Molecular Genetics, Neurophysiology and Behavior Group, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 7224, 75005 Paris, France.

2. Institut National de la Santé et de la Recherche Médicale (INSERM) U952S, 75005 Paris, France.

3. Université Pierre et Marie Curie, 75005 Paris, France.

4. Laboratory of Excellence (Labex) Biological Psychiatry Laboratory, 75005 Paris, France.

5. Neurophysiology and Behavior Group, CNRS UMR7102, 75005 Paris, France.

6. Neurotransmission and Development Group, INSERM U839, 75005 Paris, France.

7. Physiopathology of Addiction and Relapse Group, CNRS UMR7224, 75005 Paris, France.

8. Molecular and Cellular Mechanisms of Cortical Development Group, INSERM U839, 75005 Paris, France.

Abstract

Defeat, Distress, and Glucocorticoids Understanding how individuals control emotions and cope with stressful events is a major clinical concern and of importance for the treatment of psychiatric illnesses (see the Perspective by McEwen ). Barik et al. (p. 332 ) discovered that aggressive defeat stress in mice caused glucocortioid release and increased activity in the dopamine system. Deleting the glucocorticoid receptors in dopaminoceptive neurons completely prevented the social avoidance that usually follows aggressive defeat. How the combination of genetic factors and environmental stressors during adolescence determines adult behavior and how their disturbance results in neuropsychiatric disorders is poorly understood. Niwa et al. (p. 335 ) found that isolation stress during adolescence, which does not cause any long-lasting changes in wild-type mice, induced significant neurochemical and behavioral alterations in mutant mice expressing a dominant-negative variant of the disrupted in schizophrenia 1 gene under the control of the prion protein promoter. These deficits could be reversed by a glucocorticoid receptor antagonist.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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