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.