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Defense of Adrenocorticosteroid Receptor Expression in Rat Hippocampus: Effects of Stress and Strain¹

Department of Anatomy and Neurobiology (J.P.H.), University of Kentucky Medical Center, Lexington, Kentucky 40536-0084; Mental Health Research Institute (S.J.W.), University of Michigan, Ann Arbor, Michigan 48109; and Department of Psychology (R.L.S.), University of Colorado, Boulder, Colorado 80309

Address all correspondence and requests for reprints to: James P. Herman, Ph.D., Department of Anatomy and Neurobiology, University of Kentucky Medical Center, 800 Rose Street, Lexington, Kentucky 40536-0084. E-mail: jpherm00{at}pop.uky.edu

Neuronal mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) proteins are glucocorticoid-activated transcription factors that bind identical DNA response elements yet transduce distinct physiological/transcriptional actions. The present study assessed regulation of adrenocorticosteroid receptor RNA and protein following intermittent stress exposure, using Sprague Dawley (S-D) and stress-hyperresponsive Fischer 344 (F344) rat strains. The F344 (but not S-D) strain showed enhanced acute stress responsivity and enhanced corticosterone secretion following prolonged stress. F344 rats also showed reduced responsiveness to a novel stressor after prolonged stress exposure, suggestive of enhanced glucocorticoid negative feedback. Upon prolonged stress, F344 rats down-regulated MR hnRNA in CA1, CA3, and dentate gyrus. Transcriptional changes were accompanied by decreased expression of the 5' messenger RNA (mRNA) form, consistent with altered promoter utilization. In contrast, ß 5' splice variant, full-length mRNA, and MR protein expression were not affected by stress in either strain, implying that transcriptional changes do not affect overall mRNA or protein expression. GR protein was increased in pyramidal and granule cell somata/nuclei of F344 rats despite lack of a change in mRNA expression. These data suggest that prolonged stress elicits restricted changes in MR and GR expression in the F344 strain only. Overall, stable expression of adrenocorticosteroid receptors is rigorously defended in hippocampal neurons, apparently through transcriptional and posttranscriptional mechanisms.

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