Involvement of protein kinase C and arachidonic acid pathways in the gonadotropin-releasing hormone regulation of oocyte meiosis and follicular steroidogenesis in the goldfish ovary

Biol Reprod. 2002 Mar;66(3):813-22. doi: 10.1095/biolreprod66.3.813.

Abstract

The involvement of protein kinase C (PKC) and arachidonic acid (AA) pathways were investigated in the GnRH regulation of oocyte meiosis and follicular testosterone production in the goldfish ovary. The results clearly demonstrate differences in the postreceptor mechanisms involving the stimulatory and inhibitory actions of GnRH peptides on basal and gonadotropin (GtH)-induced reinitiation of oocyte meiosis and steroidogenesis. In isolated goldfish follicles in vitro, the observed stimulatory effects of both salmon GnRH (sGnRH) and chicken GnRH-II (cGnRH-II) on germinal vesicle breakdown were completely blocked by addition of PKC inhibitors, suggesting the involvement of PKC, presumably through activation of phospholipase C/diacylglycerol pathways in the GnRH-induced reinitiation of oocyte meiosis. Administration of an AA metabolism inhibitor, however, only blocked the stimulatory effect of sGnRH without affecting cGnRH-II-induced meiosis. As observed previously, in the presence of GtH, sGnRH was found to inhibit GtH-induced resumption of meiosis and testosterone production, whereas cGnRH-II was without effect. The inhibitory effect of sGnRH on GtH-induced meiosis and steroidogenesis was completely reversed by addition an AA metabolism inhibitor, whereas PKC inhibitors had no effect. These findings provide functional evidence in support of the novel hypothesis that goldfish ovarian follicles contain GnRH-receptor subtypes with different ligand selectivity mediating stimulatory and inhibitory actions of sGnRH and cGnRH in the goldfish ovary.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / pharmacology
  • 5,8,11,14-Eicosatetraynoic Acid / pharmacology
  • Animals
  • Arachidonic Acid / antagonists & inhibitors
  • Arachidonic Acid / metabolism*
  • Enzyme Inhibitors / pharmacology
  • Female
  • Goldfish / metabolism*
  • Gonadotropin-Releasing Hormone / analogs & derivatives
  • Gonadotropin-Releasing Hormone / pharmacology
  • Gonadotropin-Releasing Hormone / physiology*
  • Meiosis / drug effects
  • Oocytes / cytology*
  • Oocytes / drug effects
  • Ovarian Follicle / metabolism
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism*
  • Receptors, LHRH / metabolism
  • Testosterone / biosynthesis*
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Enzyme Inhibitors
  • Receptors, LHRH
  • 5,8,11,14-Eicosatetraynoic Acid
  • Arachidonic Acid
  • Gonadotropin-Releasing Hormone
  • Testosterone
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • LHRH, His(5)-Trp(7)-Tyr(8)-
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate