Induction of selective release of FSH in castrated male rats bearing an ovarian transplant by the administration of human chorionic gonadotrophin
ABSTRACT The present study was undertaken to determine whether hypothalamic differentiation is involved in the selective release of FSH during the periovulatory period using adult male rats castrated and implanted with an ovary. Adult male rats (70–90 days old) were castrated and an ovary obtained from a prepubertal female rat (26 days old) was immediately grafted subcutaneously. Four weeks later, human chorionic gonadotrophin (hCG, 10 i.u.) was injected i.v. into the experimentally manipulated rats to induce ovulatory changes in the grafted ovaries. Another group of similarly prepared rats was injected with 0·9% (w/v) NaCl solution as controls. After injection of hCG, plasma concentrations of FSH increased significantly by 6 h, reached peak values at 12 h and declined to control levels at 36 h. On the other hand, plasma concentrations of LH were reduced by 6 h and decreased further during the next 36 h. An abrupt fall in plasma concentrations of oestradiol-17β occurred within 3 h of the administration of hCG. Histological examination revealed that ovulatory changes and luteinization of follicles were induced in grafted ovaries by 18 h after the injection of hCG. Thirty-six hours after treatment with hCG, a set of newly formed corpora lutea was observed in grafted ovaries and plasma concentrations of progesterone were raised. Treatment with oestradiol-17β did not inhibit the selective release of FSH after the administration of hCG, suggesting that the abrupt decrease in secretion of oestradiol-17β from the grafted ovary is not involved in the occurrence of the FSH surge. These results indicate that a selective release of FSH can be induced in castrated male rats bearing an ovarian transplant probably due to decreased secretion of inhibin by the luteinized follicles in the grafted ovaries. Sex differentiation of the hypothalamus is not, therefore, involved in the selective surge of FSH. J. Endocr. (1985) 106, 31–36