INTERACTIONS OF GONADAL-STEROIDS WITH BRAIN DOPAMINE AND GONADOTROPIN-RELEASING-HORMONE IN THE CONTROL OF GONADOTROPIN-II SECRETION IN THE GOLDFISH

In goldfish it is known that intraperitoneal implantation with testosterone (T) or estradiol (E2) potentiates the serum gonadotropin-II (GtH-II) response to gonadotropin-releasing hormone (GnRH) without affecting basal GtH-II levels. Since the release of GtH-II in goldfish is under a tonic dopaminergic inhibitory tone, the possibility of sex steroids modulating brain and pituitary dopamine was examined in vivo and in vitro. Implantation of females with either T or E2 (100 μg/g in solid silastic pellets) also potentiated the increase in serum GtH-II in response to the dopamine antagonist, domperidone (10 μg/g). High-performance liquid chromatography measurements showed that steroid implantation had no effect on dopamine content in the telencephalon including preoptic area, hypothalamus, and pituitary. However, the present study demonstrates that T or E2 can increase pituitary dopamine turnover rates following tyrosine hydroxylase inhibition with α-methyl-p-tyrosine (240 μg/g). In vitro perifusion of pars distalis fragments from E2- or T-treated fish also showed a potentiation of salmon GnRH (sGnRH)-induced GtH-II release compared to controls. However, exposure to pituitary fragments from control and steroid-treated fish to increasing doses of the dopamine agonist LY 171555 did not demonstrate a significant difference in the sensitivity of the gonadotrophs to dopamine. Testosterone-induced alterations in DA turnover are dissociable from the positive action of T on pituitary responsiveness, since the potentiating effect of T implantation was not affected by severe depletion of brain and pituitary DA levels by α-methyl-p-tyrosine pretreatment. These data demonstrate that in gonad-intact goldfish, sex steroids enhance pituitary responsiveness to GnRH but basal serum GtH-II levels are maintained by a concomitant increase in DA turnover in the pituitary. © 1993 by Academic Press, Inc.