Adolescent Stress–Induced Epigenetic Control of Dopaminergic Neurons via Glucocorticoids

Author:

Niwa Minae123,Jaaro-Peled Hanna2,Tankou Stephanie2,Seshadri Saurav2,Hikida Takatoshi24,Matsumoto Yurie13,Cascella Nicola G.2,Kano Shin-ichi2,Ozaki Norio3,Nabeshima Toshitaka156,Sawa Akira2

Affiliation:

1. Department of Chemical Pharmacology, Meijo University Graduate School of Pharmaceutical Sciences, Nagoya 468-8503, Japan.

2. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.

3. Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya 464-8601, Japan.

4. Medical Innovation Center, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan.

5. Academic Frontier Project for Private University, Comparative Cognitive Science Institution, Meijo University, Nagoya 468-8503, Japan.

6. Department of Regional Pharmaceutical Care and Science, Meijo University, Nagoya 468-8503, Japan.

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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