Journal
NEUROENDOCRINOLOGY
Volume 83, Issue 5-6, Pages 371-379Publisher
KARGER
DOI: 10.1159/000096092
Keywords
Glucocorticoid; Adrenalectomy; Hippocampus; Glutamate; Hybridization, in situ; Radioimmunocytochemistry
Categories
Funding
- University of South Carolina Research Foundation
- [MH41256]
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH041256, R37MH041256] Funding Source: NIH RePORTER
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Background: In the rat hippocampus, the predominate glutamate transporters are GLT-1 and its recently identified isoform, GLT-1b. Chronic restraint stress increases GLT-1b expression throughout the hippocampus while more selectively increasing GLT-1 expression in the CA3 region. These studies suggest that GLT-1b expression is regulated by stress levels of glucocorticoids (GCs) and GLT-1 expression is regulated by stress-induced increases in extracellular glutamate levels in the CA3 region. Methods: In order to differentiate between the actions of GCs and glutamate, we examined GLT-1 isoform expression in adrenalectomized (ADX) rats and rats exposed to stress levels of GCs. Results: ADX rats revealed no significant differences in GLT-1b mRNA or protein levels compared to sham-operated controls or ADX rats given GC replacement. However, rats exposed to stress levels of GCs exhibited increases in GLT-1b protein expression in the CA3 region and the dentate gyrus. GLT-1 mRNA expression was increased by ADX, increases that were inhibited by GC replacement. Similarly, stress levels of GCs increased GLT-1 protein expression throughout the hippocampus. Conclusions: Taken together, these data indicate that GLT-1b protein expression is regulated by stress levels of GCs while the regulation of GLT-1 mRNA and protein expression provides another example of the biphasic actions of GCs in the central nervous system. Copyright (C) 2006 S. Karger AG, Basel
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