Gonadotropin releasing hormone: Regulation of phospholipid turnover and prostaglandin production in ovarian granulosa cells

The direct effect of gonadotropin releasing hormone (GnRH) upon ovarian function, is initiated by a rapid receptor-mediated increase in phosphatidylinositol (PI) turnover (^∼ 5 min) followed by prostaglandin E (PGE, 120 min) and progesterone (120 min) formation, oocyte maturation and induction of ovulation. In contrast, luteinizing hormone (LH) stimulation of oocyte maturation and induction of ovulation is mediated by increased adenosine 3′,5′-monophosphate (cAMP, 15 min), progesterone (30 min) and PGE (180 min) production. Both LH and GnRH stimulation of oocyte maturation are inhibited by dibutyryl cAMP and 3-isobutyl-1-methylxanthine, whereas induction of ovulation by the two hormones is blocked by indomethacin. GnRH and LH differ, therefore, in the mechanism leading to PGE formation, but thereafter share a common mechanism responsible for oocyte maturation and independently for induction of ovulation.