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 micrograms/g in solid silastic pellets) also potentiated the increase in serum GtH-II in response to the dopamine antagonist, domperidone (10 micrograms/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 alpha-methyl-p-tyrosine (240 micrograms/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 alpha-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.
Trudeau
V L
VL
Department of Zoology, University of Alberta, Edmonton, Canada.
Sloley
B D
BD
Wong
A O
AO
Peter
R E
RE
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D004294:Domperidone / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism*; D004343:Drug Implants; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D006054:Goldfish / Q000502:physiology*; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives / Q000494:pharmacology; D006065:Gonadotropins, Pituitary / Q000378:metabolism*; D010529:Peritoneal Cavity; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism; D013687:Telencephalon / Q000187:drug effects / Q000378:metabolism; D013739:Testosterone / Q000494:pharmacology*; D014446:Tyrosine 3-Monooxygenase / Q000037:antagonists & inhibitors
D004343:Drug Implants; D006065:Gonadotropins, Pituitary; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D004958:Estradiol; D004294:Domperidone; D014446:Tyrosine 3-Monooxygenase; D004298:Dopamine