Glucocorticoid Regulation of GLT-1 Glutamate Transporter Isoform Expression in the Rat HippocampusAutry A.E.a · Grillo C.A.a, c · Piroli G.G.a, c · Rothstein J.D.b · McEwen B.S.c · Reagan L.P.a, c
aDepartment of Pharmacology, Physiology and Neuroscience, School of Medicine, University of South Carolina, Columbia, S.C., bDepartment of Neurology and Neuroscience, Johns Hopkins University, Baltimore, Md., and cHarold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, Rockefeller University, New York, N.Y., USA
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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.
© 2006 S. Karger AG, Basel
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