Estrogen receptor-β immunoreactivity in luteinizing hormone-releasing hormone neurons of the rat brain

Feedback regulation of luteinizing hormone-releasing hormone (LHRH) neurons by estradiol plays important roles in the neuroendocrine control of reproduction. Recently, we found that the majority of LHRH neurons in the rat contain estrogen reteptor-beta (ER-beta) mRNA. whereas, they seemed to lack ER alpha mRNA expression. In addition, we observed nuclear uptake of I-125-estrogen by a subset of these cells. These data suggest that ER-beta is the chief receptor isoform mediating direct estrogen effects upon LHRH neurons. To verify the translation of ER-beta protein within LHRH cells, the present studies applied dual-label immunocytochemistry (ICC) to free-floating sections obtained from the preoptic area of rats. The improved ICC method using the silver-gold intensification of nickel-diaminobenzidine chromogen, enabled the observation of nuclear ER-beta -immunoreactivity in the majority of LHRH cells. The incidence of ER-beta expression was similarly high in LHRH neurons of ovariectomized female (87.8 +/-2.3%, mean +/- SEM). estradiol-primed female (74.9 +/-3.2%) and intact male (85.0 +/-4.7%) rats. The presence of ER-beta mRNA, ER-beta immunoreactivity and I-125-estrogen binding sites in LHRH neurons of the rat provide strong support For the notion that these cells are directly regulated by estradiol, through ER-beta. The gene targets and molecular mechanisms of this regulation remain unknown.