Effects of prostaglandin synthesis inhibitor, indomethacin on estrogen- and estrogen plus progesterone-induced sexual receptivity in ovariectomized rats.
Implants of crystalline PGE2 in the basal preoptic-anterior hypothalamic areas stimulates high levels of sexual receptivity in ovariectomized, estrogen-primed rats. Indomethacin, which blocks the synthesis of PGE2 failed to inhibit either estrogen- or estrogen plus progesterone-induced receptivity. Neither intracerebral nor subcutaneous administration of indomethacin diminished the display of steroid induced reproductive behavior without also causing a depression in open-field activity, and in some cases, causing gastrointestinal problems and even death. These results suggest the prostaglandin synthesis is not a required step in the mechanism by which estrogen and progesterone exert their behavioral effects. The possibility that PGE2 and LH-RH synthesis and/or release might contribute to a collateral mechanism for the induction of sexual receptivity was discussed.
D000818:Animals; D002369:Castration; D004347:Drug Interactions; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D007213:Indomethacin / Q000494:pharmacology*; D011374:Progesterone / Q000494:pharmacology*; D011458:Prostaglandins E / Q000096:biosynthesis / Q000494:pharmacology; D051381:Rats; D012726:Sexual Behavior, Animal / Q000187:drug effects*
D004967:Estrogens; D011458:Prostaglandins E; D011374:Progesterone; D007213:Indomethacin