Abstract

s / Journal of Equine Veterinary Science 31 (2011) 230-356 308 [7] Bilby TR, Block J, do Amaral BC, Sa Filho O, Silvestre FT, Hansen PJ, Staples CR, Thatcher WW. Effects of dietary unsaturated fatty acids on oocyte quality and follicular development in lactating dairy cows in summer. J Dairy Sci 2006;89:3891-903. Estradiol stimulation of prolactin secretion in horses: Interaction with type of secretagogue D.L. Thompson, Jr., S.E. Clavier, P.B. Mitcham, and L.R. Earl LSU Agricultural Center, Louisiana Agricultural Experiment Station, Baton Rouge, LA, U.S.A Introduction: Combining estradiol pretreatment with administration of a dopamine antagonist, such as sulpiride or domperidone, greatly enhances prolactin secretion in horses relative to treatment with either estradiol or dopamine antagonist alone [1-3]. Kelley et al. [2] first used this combination to stimulate ovarian activity and ovulation in seasonally anovulatory mares. Given that both day-to-day secretion (blood levels) of prolactin are stimulated in the long-term (weeks), as well as the immediate release of hormone in response to a testing dose of sulpiride, it is concluded that production rates of prolactin in the pituitary gland must be greatly enhanced by the combined treatment. The current experiments were designed to determine whether secretagogues other than dopamine antagonists would interact with estradiol pretreatment in the same manner. Materials and Methods: Two experiments were conducted. The first (July, 2009) tested the effects of estradiol pretreatment in geldings on the prolactin responses to exercise, epinephrine injection, prostaglandin-F2 a (Lutalyse; animalhealth.pfizer. com) injection, and sulpiride injection. Six geldings were administered estradiol cypionate (ECP; betlabs.com) and six geldings were administered vegetable oil on day 0. All geldings were exercised (trotting for 5 min at hourly intervals for a total of 4 bouts) on day 5, were administered epinephrine at 5 mg/kg BW i.v. on day 7, were administered 10 mg Lutalyse i.v. on day 10, and were administered sulpiride (0.1 mg/kg BW i.v.) on day 12. Prolactin was measured in blood samples collected immediately before and at frequent intervals after each treatment. The second experiment (February, 2010) tested the effects of daily administration of thyrotropin releasing hormone (TRH) and(or) ECP on daily prolactin concentrations in a 2 x 2 factorial design with 4 geldings per subgroup. Half the geldings received 50 mg ECP i.m. on day 0 and the rest received vegetable oil. Starting on day 10, half of each of those groups received either daily TRH injections (1.5 mg i.m) or saline injections of similar volumes. The TRH-saline injections were repeated through day 30. Prolactin was measured in all samples with previously validated RIA [4]. Data in each experiment were analyzed via ANOVA in SAS in repeatedmeasures designs. Differences between groups within time periods were assessed by the LSD test. Results and Discussion: In the first experiment, ECP treatment increased (P 1⁄4 .07) plasma prolactin concentrations before the onset of exercise, and exercise stimulated (P < .001) plasma prolactin concentrations after each bout. There was no interaction with estradiol pretreatment. Epinephrine did not alter prolactin concentrations. Lutalyse administration stimulated (P < .001) prolactin concentrations, but there was no interaction with ECP pretreatment. Sulpiride administration stimulated (P < .001) prolactin concentrations, and there was a greater (P 1⁄4 .038) response in ECP-treated geldings relative to controls. In the second experiment, ECP administration did not affect prolactin concentrations. Injection of TRH stimulated prolactin concentrations on the first day of injection, but had no effect on prolactin concentrations otherwise. There was no interaction of ECP and TRH administration either on the prolactin response on the first day of TRH injection, or across the 20 days of treatment. Conclusion: Unlike the synergistic interaction of estradiol pretreatment and dopamine antagonist administration on prolactin secretion, there was no interaction of ECP and other types of prolactin secretagogues in the first experiment. Even though exercise and Lutalyse stimulated prolactin secretion, it was equally stimulated in ECP-treated and control geldings; subsequent administration of sulpiride revealed that the estradiol-dopamine antagonist interaction existed in the same geldings 2 days later. In some way, the mechanism of release of prolactin from estradiol-stimulated lactotropes differs for dopamine antagonists and other prolactin-releasing stimuli. This would indicate that the stimulus for prolactin secretion after exercise or Lutalyse is not a reduction in dopamine input to the pituitary gland. Unlike sulpiride or domperidone, daily TRH injection after ECP pretreatment did not stimulate long-term prolactin secretion. Thus, even though TRH is a secretagogue for prolactin, it is unable to enhance prolactin production in combination with estradiol stimulation. 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, appears to be limited to dopamine antagonists.

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