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Decrements in Nuclear Glucocorticoid Receptor (GR) Protein Levels and DNA Binding in Aged Rat Hippocampus

Department of Psychiatry, University of Cincinnati Medical Center (E.K.M., J.P.H.), Cincinnati, Ohio 45267-0559; Anatomy and Neurobiology, University of Kentucky School of Medicine (K.J.S., J.P.H.), Lexington, Kentucky 40536-0084; and Department of Psychology, University of Colorado (R.L.S.), Boulder, Colorado 80309

Address all correspondence and requests for reprints to: James P. Herman, Ph.D., Department of Psychiatry, University of Cincinnati, 231 Albert Sabin Avenue, Cincinnati, Ohio 45267-0559. E-mail: . jpherman{at}psychiatry.uc.edu

Hippocampal glucocorticoid receptors (GRs) are believed to play a major role in age-related cognitive decline and cellular vulnerability. It has been proposed that these receptors mediate damaging effects of elevated glucocorticoid secretion on cellular function. In the present report we present evidence that intracellular trafficking of the GR is impaired with hippocampal aging, manifest as decreased nuclear translocation and deficient DNA binding. We also present evidence that chaperone proteins responsible for GR nuclear translocation are decreased with hippocampal aging. Age-related nuclear GR decreases are not observed in hypothalamus, indicating regional specificity of trafficking deficits. Aging did not affect nuclear or cytosolic MR levels. These data suggest that GR signaling is diminished, rather than enhanced, during hippocampal aging. Diminished GR signaling capacity may attenuate the beneficial effects of glucocorticoids on hippocampal regulation of memory and stress integration.

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