TESTOSTERONE ENHANCES GABA AND TAURINE BUT NOT N-METHYL-D,L-ASPARTATE STIMULATION OF GONADOTROPIN-SECRETION IN THE GOLDFISH - POSSIBLE SEX STEROID FEEDBACK MECHANISMS

The effects of gonadal steroids on GABA-, taurine (TAU)- and N-methyl-D,L-aspartate (NMA)-induced gonadotropin-II (GTH-II) release were investigated in male and female goldfish in vivo. In sexually regressed goldfish (both sexes mixed), intraperitoneal implantation for 5 to 10 days with solid Silastic pellets containing testosterone (100 mug/g), oestradiol (100 mug/g) or progesterone (100 mug/g) was previously shown to elevate serum sex steroid levels to values comparable to those in sexually mature animals, and to potentiate gonadotropin-releasing hormone-stimulated GTH-11 release. In the present study, testosterone but not oestradiol or progesterone enhanced the stimulatory effects of exogenous GABA (100 mug/g) on GTH-II release in vivo. TAU (1 mg/g) stimulated GTH-II release in sexually regressed mixed sex and sexually recrudescent male goldfish, and both testosterone and oestradiol implantation enhanced GTH-II release induced by TAU. The glutamate agonist NMA (25 to 50 mug/g) was also found to stimulate GTH-II release; however it was relatively less effective in elevating serum GTH-II levels than GABA and TAU, and its effects were not modulated by sex steroid treatments. Pretreatment of goldfish with alpha-methyl-p-tyrosine to deplete brain and pituitary catecholamines did not affect NMA action on GTH-II release. Our results indicate that GABA, TAU and NMA are involved in the neuroendocrine regulation of GTH-II release in goldfish, and support the idea that testosterone participates in the positive feedback regulation of pituitary gonadotropin release in a non-mammalian vertebrate by enhancing GABA- and TAU-stimulated GTH release in vivo.