Early life adversity is known to have profound effects on the development and function
of neural circuits that control emotional behaviors (
1
). The result in humans is a greatly enhanced predisposition to develop depression
and anxiety disorders or addiction throughout the individual's lifetime. Rodent models
of chronic stress have begun to identify the critical periods of early life adversity
along with the brain circuits and molecules that control pathologic behaviors relevant
to these psychiatric disorders. In this issue, Wei et al. (
2
) provides new evidence for a critical window before weaning, whereby increased levels
of glucocorticoid receptors (GRs) in the forebrain lead to lifelong increases in exploratory-based
anxiety behavior and cocaine-induced locomotor sensitization. Associated with these
behavioral changes are vast lifelong transcriptional changes in the dentate gyrus
of the hippocampus (hipp) and, to a lesser extent, the nucleus accumbens (NAc), brain
structures critically involved in stress disorders and addiction. These data highlight
the potential importance of developmental experience in controlling normal brain function
and behavior in adulthood.To read this article in full you will need to make a payment
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References
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Article info
Publication history
Accepted:
November 30,
2011
Received:
November 29,
2011
Identification
Copyright
© 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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- Early-Life Forebrain Glucocorticoid Receptor Overexpression Increases Anxiety Behavior and Cocaine SensitizationBiological PsychiatryVol. 71Issue 3
- PreviewGenetic factors and early-life adversity are critical in the etiology of mood disorders and substance abuse. Because of their role in the transduction of stress responses, glucocorticoid hormones and their receptors could serve as both genetic factors and mediators of environmental influences. We have shown that constitutive overexpression of the glucocorticoid receptor (GR) in forebrain results in increased emotional reactivity and lability in mice. Here, we asked whether there was a critical period for the emergence of this phenotype.
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