Dopamine D2 receptors and secretion of FSH and LH: role of sexual steroids on the pituitary of the female rainbow trout

Gen Comp Endocrinol. 2002 Jun 15;127(2):198-206. doi: 10.1016/s0016-6480(02)00046-1.

Abstract

The role of sexual steroids in the modulation of a dopaminergic inhibitory tone on FSH and LH release was studied in the rainbow trout. The experiments were performed on previtellogenic trout, implanted or not with estradiol (E(2)), and vitellogenic trout. E(2) implant increased the circulating levels of LH and decreased the circulating levels of FSH in previtellogenic fish. The catecholamine inhibitor alphaMPT increased the circulating levels of LH, implanted or not with E(2). AlphaMPT increased circulating levels of LH in vitellogenic fish. This increase could be prevented by the dopaminergic agonist bromocryptine. The dopaminergic drugs had no effect on the circulating levels of FSH in all groups. E(2) decreased mRNA levels of sGnRH1 and sGnRH2 in the telencephalon of previtellogenic fish. The dopaminergic treatments had no effect on mRNA levels of both forms of sGnRH in previtellogenic and vitellogenic fish. Primary cultures of pituitary cells were primed for three days with steroids (E(2) or 17alpha-hydroxy, 20beta-dihydroprogesterone (17alpha20betaP)) before treatment with increasing doses of bromocryptine, associated or not with sGnRH. E(2), but not 17alpha20betaP, potentiated the sGnRH-induced release of LH. Bromocryptine induced a slight dose-dependent decrease of sGnRH-induced release of LH. This decrease was potentiated by 17alpha20betaP. E(2) and 17alpha20betaP had no effect on the release of FSH, but bromocryptine decreased the 10(-8)M sGnRH-induced release of FSH. In conclusion, the development of the dopaminergic inhibitory tone on gonadotropin release, at the onset of vitellogenesis, requires factors other than estradiol. E(2) should contribute in part to decrease the release of FSH. At the end of the reproductive cycle, 17alpha20betaP should reinforce the dopaminergic inhibitory tone.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Chemistry / physiology
  • Bromocriptine / pharmacology
  • Cells, Cultured
  • DNA, Complementary / metabolism
  • Dopamine / metabolism
  • Dopamine Agonists / pharmacology
  • Dose-Response Relationship, Drug
  • Estradiol / pharmacology
  • Female
  • Follicle Stimulating Hormone / metabolism*
  • Gonadal Steroid Hormones / physiology*
  • Gonadotropin-Releasing Hormone / pharmacology
  • Hydroxyprogesterones / pharmacology
  • Luteinizing Hormone / metabolism*
  • Oncorhynchus mykiss / metabolism*
  • Pituitary Gland / metabolism*
  • Receptors, Dopamine D2 / metabolism*

Substances

  • DNA, Complementary
  • Dopamine Agonists
  • Gonadal Steroid Hormones
  • Hydroxyprogesterones
  • Receptors, Dopamine D2
  • 17 alpha,20 beta-dihydroxypregn-4-en-3-one
  • Gonadotropin-Releasing Hormone
  • Bromocriptine
  • Estradiol
  • Luteinizing Hormone
  • Follicle Stimulating Hormone
  • Dopamine