Effects of sex steroid treatments on gonadotropin-releasing hormone-stimulated gonadotropin secretion from the goldfish pituitary.

Abstract

The effects of gonadal steroids on the gonadotropin (GTH) release response to salmon gonadotropin-releasing hormone (sGnRH), chicken gonadotropin-releasing hormone-II (cGnRH-II), and the sGnRH analogue, [D-Arg6, Trp7, Leu epsilon, Pro9]-N-ethylamide-GnRH (sGnRH-A), were investigated using an in vitro perifusion system for goldfish pituitary fragments. Gonad-intact male and female goldfish were implanted intraperitoneally (i.p.) with silastic pellets containing no steroid (blank), testosterone (T; 100 micrograms/g), or estradiol (E2; 100 micrograms/g); pituitaries were removed 5 days later for perifusion experiments. In vivo treatment with T or E2 potentiates sGnRH-, cGnRH-II-, and sGnRH-A-induced GTH secretion from pituitary fragments of sexually regressed and sexually recrudescent goldfish in vitro. Testosterone (100 nM; 24 h) treatment in vitro has a direct effect on the pituitary to increase sGnRH responsiveness, and this potentiating effect of T was blocked by the protein synthesis inhibitor cycloheximide (25 microM). In sexually regressed goldfish, in vivo T implantation enhanced the serum GTH response to sGnRH-A (0.01 microgram/g; 6 h) 7-fold. ED50 estimates for in vitro pituitary GTH responsiveness to sGnRH-A were 1.0 +/- 0.1 nM and 0.1 +/- 0.1 nM (p < 0.05) for blank and T-implanted groups, respectively. Radioligand (125I-sGnRH-A) binding studies demonstrated that enhanced pituitary responsiveness was independent of changes in pituitary GnRH receptor affinity or number. These results demonstrate that sex steroids increase pituitary sensitivity to GnRH peptides in the goldfish.