Influences of luteinizing hormone releasing hormone, hypophysectomy and orchidectomy on the differentiation of luteinizing hormone and follicle-stimulating hormone cells and in an ectopic pituitary in the hamster.

Abstract

In these experiments we examined the effects of luteinizing hormone releasing hormone (LHRH) and gonadal and pituitary hormones on the appearance of luteinizing hormone (LH) and follicle-stimulating hormone (FSI-I) cells in ectopic pituitaries in the hamster. As a reference, we first determined the sequence of appearance of these hormones in perinatal animals using immunohistochemical (IHC) and radioimmunoassay (RIA) procedures. Neither hormone could be detected in pituitaries at 13 days of gestation by either technique. Both hormones could be detected by IHC at 15 days of gestation using anti-rat LH S4, anti-rat LH�3, anti-rat FSH S-7, and anti-rat FSI-Ia antisera. Il-IC and RIA revealed an increase in gonadotroph population and gonadotrophin content, respectively, between 5 and 12 days of postnatal life. By Day 8 a sex difference emerged with RIA so that by Day 12 both pituitary LH and FSH content were higher in females. In serum, only FSH was higher in females. To study the determinants of gonadotroph differentiation, fetal (Days 13-15 of gestation) or postnatal pituitaries (<3 days) were transplanted to a site remote from the hypothalamus (beneath the renal capsule) of hosts whose endocrine state could be manipulated easily (adult male hamsters). The hosts were intact, hypophysectomized, orchidectomized, or hypophysectomizedorchidectomized hamsters. Some hosts were also treated with LHRH (dosages of 5, 30 or 50 Mg/day for 4, 12 or 19 days). In grafts of any hosts not treated with LHRH, the number of detectable FSH cells was always much less than the number of LH cells. LHRH treatment of any host increased the number of LH and FSH cells detected. After 19 days of treatment, the numbers of LH and FSH cells identified were approximately equal. Both gonadotrophins often were found in the same cell. In nonhypophysectomized hosts, with or without testes, LHRH often produced a significant depression of serum LH when measured 16 h after the last injection. Although LHRH did not alter basal serum LH levels in hypophysectomized hosts 16 h after the last injection, it did elevate serum LH in similar hosts forat least3 h after the injection. In nonhypophysectomized hosts with testes, LHRH significantly elevated serum FSH levels. However, LHRFI did not alter serum FSH in orchidectomized hosts. A tendency for LHRH to increase basal serum FSH levels in hypophysectomized or hypophysectomized-orchidectomized hosts existed. These experiments revealed that when pituitaries were removed from perinatal hamsters and placed in an ectopic site the accumulation of intracellular LH was greater than FSH. This result was not affected by hypophysectomy and/or orchidectomy of the hosts. The resemblance of the development of gonadotrophs in the in situ pituitary with that in ectopic pituitaries in hosts treated with LHRH suggests that LHRH may be a major determinant of normal gonadotroph differentiation.