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Effects of nafoxidine on the luteinizing hormone surge: temporal distribution of estrogen receptors and induction of cytoplasmic progestin receptors in the hypothalamus-preoptic area, pituitary, and uterus of the immature rat

, : Effects of nafoxidine on the luteinizing hormone surge: temporal distribution of estrogen receptors and induction of cytoplasmic progestin receptors in the hypothalamus-preoptic area, pituitary, and uterus of the immature rat. Endocrinology 109(5): 1365-1374

The antiestrogen nafoxidine 1-(2-[P-(3,4-dihydro-6-methoxy-2-phenyl-1-naphthyl)phenoxy]pyrrolidine hydrochloride; 2 mg/rat), blocked LH surges induced by Silastic implants containing estradiol (E2) in oil (150 micrograms/ml) in the immature female rat and had no stimulatory effect on gonadotropin secretion by itself. Furthermore, the administration of progesterone (P) to rats primed for 24 h with nafoxidine alone or nafoxidine plus E2 did not lead to premature and enhanced LH surges (facilitation) as it does in E2-primed animals. Pituitary LH content was depleted by 30-50% after E2-induced or P-facilitated LH surges, but was unchanged after the administration of nafoxidine or nafoxidine plus E2. To investigate the cellular mechanisms involved, levels of total cytoplasmic and nuclear estrogen receptors and cytoplasmic progestin receptors in the hypothalamus-preoptic area (HPOA), pituitary, and uterus were measured by [3H]E2 or [3H]R5020 (3H-labeled 17,21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione) exchange assays at various times after the administration of E2 and /or nafoxidine. The ability of nafoxidine to bind in vitro to cytoplasmic or nuclear estrogen receptors was, respectively, 4% and 2% (HPOA), 5% and 6% (pituitary), and 1% and 2% (uterus) relative to E2 (100%). After the injection of nafoxidine or the insertion of E2 implants, cytoplasmic estrogen receptors were depleted with a similar time course and remained depressed for at least 48 h in both the HPOA and pituitary. In the uterus, the antiestrogen prevented the replenishment of cytoplasmic estrogen receptors observed in response to E2. Nuclear estrogen receptor levels in the HPOA and pituitary peaked 1 h after E2 and subsequently declined to a plateau from 24-48 h (at 2-4 times the levels found in untreated rats). After nafoxidine, accumulation of these receptors in the nucleus was more gradual and prolonged. Absolute levels of estrogen receptors translocated to the nucleus by E2 or nafoxidine were comparable. E2 treatment led to a substantial induction of cytoplasmic progestin receptors (approximately 2-fold in the HPOA, approximately 4-fold in the pituitary, and approximately 7-fold in the uterus after 48 h), and this process was considerably inhibited by nafoxidine. These results support the notions that antagonism by nafoxidine of estrogen action may be due to a defective association of the antiestrogen-receptor complex with nuclear sites, ad progestin receptor induction may be a prerequisite for the facilitation of gonadotropin surges by P.


PMID: 7297482

DOI: 10.1210/endo-109-5-1365

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