Effects Of Dopamine Norepinephrine, Serotonin And Estradiol-17-Beta On Secretion Of Luteinizing Hormone And Prolactin In The Ewe.

Four studies were conducted to determine effects of dopamine (DA), norepinephrine (NE), serotonin (5-HT) and estradiol-17(beta) on secretion of luteinizing hormone (LH) and prolactin (PRL) in ewes. In the first study, tonic and LHRH-induced secretion of LH was affected by intravenous infusion of DA, NE and 5-HT in a dose-dependent manner in ovariectomized ewes. Responses of LH to increasing doses of DA and 5-HT were biphasic and slopes of dose-response curves between catecholamines and 5-HT were opposite. Secretion of PRL was inhibited by DA and NE but not affected by 5-HT. In anestrous ewes no effects of DA, NE and 5-HT were noted on tonic secretion of LH. However, NE inhibited and 5-HT enhanced LHRH-induced release of LH, independent of the dose of NE or 5-HT infused. In anestrous ewes DA and NE inhibited secretion of PRL. In the second study, tonic secretion of LH was inhibited by DA and enhanced by 5-HT following induction of luteal regression with prostaglandin F(,2)(alpha). Neither DA nor 5-HT affected the pre-ovulatory surge of LH. Concentrations of estradiol-17(beta) in plasma were reduced by DA and this effect was reversed partially by 5-HT. In a third experiment, patterns of LH differed between acutely overiectomized ewes with implants of estradiol-17(beta) and ewes in which only the corpus luteum was removed. Following lutectomy a surge of PRL was associated with the preovulatory surge of LH. In ovariectomized ewes with implants of estradiol-17(beta), the magnitude of the surge of LH was less than that observed for lutectomized ewes; no surge of PRL accompanied the surge of LH. In the fourth study, treatment of ovariectomized ewes with estradiol-17(beta) during the summer increased the magnitude of the release of LH following LHRH. This increased release of LH was inhibited by para-chlorophenylalanine (PCPA), an inhibitor of 5-HT synthesis. The effect of PCPA was reversed partially by quipazine, an agonist of 5-HT. Treatment of non-estradiol-17(beta) treated ovariectomized ewes with quipazine or PCPA increased release of LH after LHRH. Key findings of these studies included: (1) in ovariectomized ewes response of LH to DA, NE and 5-HT was dose-dependent; (2) tonic secretion of LH was inhibited by DA and enhanced by 5-HT following prostaglandin F(,2)(alpha)-induced luteolysis; (3) ovarian secretions in addition to estradiol-17(beta) affected secretion of LH and PRL; and (4) enhanced release of LH after administration of LHRH in estradiol-17(beta)-treated ovariectomized ewes was mediated by 5-HT