Estradiol Effects on Secretagogue-Induced Prolactin Release: Disparity in Responses to Sulpiride, Exercise, Epinephrine, Prostaglandin-F2α, and Thyrotropin-Releasing Hormone

Three experiments were conducted (1) to assess the effects of estradiol pretreatment on the prolactin response to various secretagogues, and (2) to determine whether elevated plasma thyroxine concentrations altered the prolactin responses to those secretagogues. Geldings were available and were used because their prolactin and luteinizing hormone responses to estradiol and dopamine antagonists are known to be similar to those in seasonally anovulatory mares. In the first experiment, performed in summer, estradiol cypionate (ECP; 100 mg) treatment of geldings increased (P = .07) plasma prolactin concentrations before the onset of exercise, and repeated exercise bouts stimulated (P < .001) plasma prolactin concentrations after each bout; there was no interaction with estradiol pretreatment. Epinephrine injection (5 μg/kg of body weight) did not alter prolactin concentrations. Prostaglandin-F2α administration (10 mg Lutalyse) stimulated (P < .001) prolactin concentrations, but there was no interaction with ECP pretreatment. Sulpiride administration (0.1 mg/kg of body weight) stimulated (P < .001) prolactin concentrations, and there was a greater (P = .038) response in ECP-treated geldings relative to controls. In the second experiment, performed in winter, ECP (50 mg) pretreatment of geldings before 21 days of daily thyrotropin-releasing hormone (TRH; 1.5 mg) injections did not alter prolactin secretion (P > .1); TRH stimulated prolactin secretion only after the very first injection. In the third experiment (performed in July), pretreatment of geldings with 50 mg of thyroxine in biodegradable particles (day 0) raised (P < .001) plasma thyroxine concentrations in plasma for the duration of the experiment, but had no effect on the prolactin responses to two exercise bouts on day 5, to an injection of prostaglandin-F2α on day 9, or to an injection of sulpiride on day 13. The previously reported stimulation of plasma prolactin concentrations by estradiol pretreatment and subsequent sulpiride administration in mares, as evidenced herein in geldings, does not occur when prolactin is stimulated by exercise, prostaglandin-F2α, or TRH. The practical impact of these data is that stimulation of prolactin concentrations after ECP treatment in winter, in an effort to stimulate ovarian activity in seasonally anovulatory mares, is likely limited to dopamine antagonists. Results of the third experiment indicate that TRH is not likely the mediator in the prolactin response to exercise or prostaglandin-F2α injection.