Journal
NEUROSCIENCE
Volume 231, Issue -, Pages 38-48Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2012.11.037
Keywords
stress; corticosterone; hippocampus; amygdala; GABA; glutamate
Categories
Funding
- Natural Sciences and Engineering Research Council of Canada
- Xunta de Galicia
- Spanish Ministry of Science and Technology
- FEDER
- Canada Research Chairs Program of Canada
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We investigated the effect of two well characterized preclinical animal models of depression - repeated injections of corticosterone (CORT) and repeated restraint stress - on markers of GABAergic and glutamatergic activity in the hippocampus and amygdala. Stress is an identified risk factor for the onset of major depression, but the neurobiological mechanisms by which stress may produce depressogenic effects are not clear. Rats received one of the following four treatments for 21 consecutive days: daily single CORT injections (40 mg/kg), daily single vehicle injections, daily 6 h of restraint stress, or daily handling. After the 21-day stress period, all rats were sacrificed and hippocampal and amygdalar tissue was collected and prepared for Western blot analyses. We examined the effect of CORT and restraint stress on glutamate decarboxylase (GAD)-65 and GAD67, as well as the alpha 1, alpha 2, alpha 3, and beta 2-3 GABA(A) receptor subunits, and the vesicular glutamate transporter (VGLUT)-2. We found that CORT significantly decreased GAD65 and the alpha 2 receptor subunit and increased VGLUT2 within the hippocampus. We also found that CORT decreased GAD67 and the alpha 2 receptor subunit in the amygdala. However, restraint stress had no significant effect on protein expression in either the hippocampus or the amygdala. These findings parallel our previous results showing that repeated CORT injections, but not restraint stress, increase depression-like behavior in rats, and suggest that the depressogenic effects of CORT may be related to alterations in GABAergic and glutamatergic neurotransmission in stress-sensitive regions of the brain. (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
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