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 receptor-β (ER-β) mRNA, whereas, they seemed to lack ER-α mRNA expression. In addition, we observed nuclear uptake of 125I-estrogen by a subset of these cells. These data suggest that ER-β is the chief receptor isoform mediating direct estrogen effects upon LHRH neurons. To verify the translation of ER-β protein within LHRH cells, the present studies applied dual-label immunocytochemistry (ICC) to freefloating 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-β-immunoreactivity in the majority of LHRH cells. The incidence of ER-β expression was similarly high in LHRH neurons of ovariectomized female (87.8±2.3%, mean±SEM), estradiol-primed female (74.95±3.2%) and intact male (85.0±4.7%) rats. The presence of ER-β mRNA, ER-β immunoreactivity and 125I-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-β. The gene targets and molecular mechanisms of this regulation remain unknown.
- Estrogen receptor
- Gonadotropin-releasing hormone
- Steroid receptor
ASJC Scopus subject areas