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)-β 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 ERβ 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 ERβ 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 ERβ 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 ERβ expression, we examined the effects of these steroids on ERβ mRNA levels using real-time RT-PCR. EB significantly decreased the expression of ERβ mRNA in the PVN (P = 0.0006) and SON (P < 0.01). In contrast, DEX did not change ERβ mRNA levels. These results indicate that glucocorticoids and estrogen exert opposing regulatory influences on the ERβ gene expression. This may represent a mechanism by which these steroids can alter the cellular sensitivity of ERβ-expressing neurons to subsequent steroidal activation.
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