Opioids modulate pituitary receptors for gonadotropin-releasing hormone.
The number of pituitary GnRH receptors (GnRH-BC) is stable throughout the day in ovariectomized-estradiol treated rats, but undergo an acute transient reduction prior to the afternoon gonadotropin surge. To investigate the mechanisms controlling GnRH-BC we studied the effects of opioid-active compounds in this model. Morphine, given at 1400h, abolished both the LH surge and the preceding fall in GnRH-BC. Morphine given at 0900h increased GnRH-BC 30 min later, and this effect was abolished by simultaneous administration of naloxone. Naloxone alone produced an acute transient fall in GnRH-BC of similar magnitude to that seen before the spontaneous LH surge. These data suggest that alterations in endogenous opioid activity can modulate GnRH receptors and may form part of the mechanisms which initiate the afternoon gonadotropin surge.
D000818:Animals; D002369:Castration; D004958:Estradiol / Q000494:pharmacology; D004971:Estrus; D005260:Female; D009270:Naloxone / Q000494:pharmacology; D009294:Narcotics / Q000494:pharmacology*; D010902:Pituitary Gland / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D011956:Receptors, Cell Surface / Q000187:drug effects*; D011966:Receptors, LHRH
D009294:Narcotics; D011956:Receptors, Cell Surface; D011966:Receptors, LHRH; D009270:Naloxone; D004958:Estradiol