Glucocorticoid regulation of GLT-1 glutamate transporter isoform expression in the rat hippocampus

Anita E. Autry, Claudia A. Grillo, Gerardo G. Piroli, Jeffrey D. Rothstein, Bruce S. McEwen, Lawrence P. Reagan

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)371-379
Number of pages9
Issue number5-6
StatePublished - Oct 2006
Externally publishedYes


  • Adrenalectomy
  • Glucocorticoid
  • Glutamate
  • Hippocampus
  • Hybridization, in situ
  • Radioimmunocytochemistry

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience


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