Effects of gonadectomy and sex steroids on pituitary gonadotrophin release and response to gonadotrophin-releasing hormone (GnRH) agonist in the bullfrog, Rana catesbeiana

Abstract

Gonadectomy of adult bullfrogs, Rana catesbeiana, elevated plasma levels of both follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Profiles of plasma gonadotrophins after gonadectomy were similar in the two sexes; however, FSH increased faster in females than males. Both gonadotrophins continued to rise for several months and remained elevated after 1 year, but there was some dissociation between the two hormones; FSH increased sooner (1 week vs 3 weeks), reached higher levels ( FSH LH ⪢ 1 ), and did not show the secondary decline exhibited in LH. Similarly, in subadult males and females, gonadectomy increased plasma FSH by 1 week but LH levels were less affected. Postgonadectomy increases in both gonadotrophins were prevented by chronic (6-week) implantation of capsules containing estradiol-17β (E 2) or 5α-dihydrotestosterone (DHT), and treatment with DHT and E 2 within physiological ranges starting 1 year after gonadectomy also suppressed chronically elevated levels of plasma gonadotrophins. Compared to untreated gonadectomized frogs, the rate of increase in both plasma gonadotrophins was accelerated after removal of DHT at 6 weeks. Acute pituitary responsiveness to a gonadotrophin-releasing hormone (GnRH) agonist was markedly reduced in short-term (3.5–8 weeks) gonadectomized subadult males (but not females) and in long-term (1 year) gonadectomized males and females. Treatment with E 2 had no effect on GnRH responsiveness in these frogs, but DHT implants significantly enhanced the response to agonist in both sexes. Thus, the nonaromatizable androgen—DHT—may have both negative feedback effects (at the hypothalamic level) and positive effects at the level of the pituitary, whereas, estrogen exhibited only the former, negative feedback activity. Sex differences in circulating DHT, which are detectable even in juveniles, may account for the sexual dimorphism in pituitary responsiveness to GnRH in the bullfrog.