Journal
SCIENCE
Volume 339, Issue 6117, Pages 335-339Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1226931
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Funding
- Stanley
- RUSK
- S-R
- NARSAD
- Maryland Stem Cell Research Fund
- NIH [MH-084018, MH-094268, MH-069853, MH-085226, MH-088753, MH-092443, K99MH-094408]
- JSPS-Korea
- Ministry of Education, Culture, Sports, Science and Technology/Ministry of Health, Labour and Welfare of Japan (MEXT/MHLW)
- JSPS [22248033, 20390073, 22659213, 20007152, 23-639]
- Strategic Research Program for Brain Sciences
- MEXT/MHLW
- Grants-in-Aid for Scientific Research [20390073, 22248033, 23680034] Funding Source: KAKEN
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Environmental stressors during childhood and adolescence influence postnatal brain maturation and human behavioral patterns in adulthood. Accordingly, excess stressors result in adult-onset neuropsychiatric disorders. We describe an underlying mechanism in which glucocorticoids link adolescent stressors to epigenetic controls in neurons. In a mouse model of this phenomenon, a mild isolation stress affects the mesocortical projection of dopaminergic neurons in which DNA hypermethylation of the tyrosine hydroxylase gene is elicited, but only when combined with a relevant genetic risk for neuropsychiatric disorders. These molecular changes are associated with several neurochemical and behavioral deficits that occur in this mouse model, all of which are blocked by a glucocorticoid receptor antagonist. The biology and phenotypes of the mouse models resemble those of psychotic depression, a common and debilitating psychiatric disease.
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