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Regulation of Estrogen Receptor-ß Expression in the Female Rat Hypothalamus: Differential Effects of Dexamethasone and Estradiol

Department of Biomedical Sciences (S.S., R.J.H.), Colorado State University, Fort Collins, Colorado 80523; and Neuroscience Program (S.S.), Loyola University Chicago, Maywood, Illinois 60153

Address all correspondence and requests for reprints to: Robert J. Handa, Ph.D., Department of Biomedical Sciences, Anatomy and Neurobiology Section, Colorado State University, 1350 Center Avenue, Fort Collins, Colorado 80523. E-mail: robert.handa{at}colostate.edu.

Estrogen and glucocorticoids interact in multiple aspects of endocrine regulation by exerting opposing influences on the expression of selective genes. In rats, estrogen receptor (ER)-ß is the predominant form of ER present in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, suggesting its involvement in neuroendocrine regulation. To date, the hormonal regulatory profile of the ERß gene in the rat central nervous system has not been closely elucidated. In the present study, we first examined the effects of dexamethasone (DEX) and estradiol benzoate (EB) on the ERß protein expression in the PVN and SON of ovariectomized female rats. In the SON and parvocellular and magnocellular parts of the PVN, the number of ERß immunoreactive nuclei significantly increased after DEX treatment, compared with the control group, whereas EB treatment caused a significant decrease. The effect of EB was consistent across other brain nuclei such as the anteroventral periventricular nucleus and medial preoptic nucleus. To determine the molecular level at which DEX and EB control ERß expression, we examined the effects of these steroids on ERß mRNA levels using real-time RT-PCR. EB significantly decreased the expression of ERß mRNA in the PVN (P = 0.0006) and SON (P < 0.01). In contrast, DEX did not change ERß mRNA levels. These results indicate that glucocorticoids and estrogen exert opposing regulatory influences on the ERß gene expression. This may represent a mechanism by which these steroids can alter the cellular sensitivity of ERß-expressing neurons to subsequent steroidal activation.

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