title: Pituitary gonadotropin-releasing hormone receptor content in rats with polycystic ovaries.
abstract: A single injection of estradiol valerate (EV) induces, after a lag period of 4-6 wk, a chronic anovulatory polycystic ovarian (PCO) condition in adult rats. This condition is associated with a selective compromise of luteinizing hormone (LH) release and/or synthesis reflected in low basal serum LH concentrations, decreased pituitary content of LH, and decreased gonadotropin-releasing hormone (GnRH)-stimulated LH secretion. The present study was undertaken to determine to what extent the aberrant LH release in rats with PCO could be related to alterations in pituitary content of GnRH receptors. Pituitary GnRH-receptor content was assessed by the evaluation of saturation binding of a GnRH analog, [125I]-D-Ala6-des-Gly10-GnRH, to pituitary membrane preparations. The receptor content of pituitaries from rats with PCO was compared to that obtained from intact animals at estrus and diestrus. Receptor levels in ovariectomized normal rats and rats with PCO were also assessed. The pituitary GnRH receptor content in PCO rats was similar to that observed in normal controls at estrus and was significantly lower than that for rats at diestrus. Although a twofold increase in pituitary GnRH receptor content was observed at 28 days following the castration of control rats, GnRH receptor content in the pituitaries of PCO rats, at 28 days following ovariectomy, remained unchanged. Although, castration-induced elevations in mean serum LH and follicle-stimulating hormone (FSH) concentrations were observed in both the PCO and control animals, the rise in both gonadotropins was significantly attenuated in the PCO-castrates when compared to the ovariectomized controls. Since GnRH is a major factor in the regulation of pituitary GnRH receptor content, these findings suggest that hypothalamic GnRH release is impaired in rats with PCO and that this impairment is independent of any influences from the polycystic ovaries.
authors.affiliation: Department of Anatomy, McGill University, Montreal, Quebec, Canada.
authors.forename: P D
authors.initials: PD
authors.lastname: Carriere
authors.forename: J R
authors.initials: JR
authors.lastname: Brawer
authors.forename: R
authors.initials: R
authors.lastname: Farookhi
mesh_terms: D000818:Animals; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood; D010052:Ovariectomy; D010053:Ovary / Q000648:ultrastructure*; D010903:Pituitary Gland, Anterior / Q000032:analysis / Q000378:metabolism; D010906:Pituitary Hormone-Releasing Hormones / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000139:chemically induced / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D011966:Receptors, LHRH / Q000032:analysis*
chemical_list: D010906:Pituitary Hormone-Releasing Hormones; D011966:Receptors, LHRH; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone