NEUROENDOCRINE REGULATION OF OVINE ESTROUS CYCLES

这项研究的长期目标是阐明神经系统的功能， 孕酮防止黄体期缩短的内分泌机制 循环在母羊。 有人提出，孕酮可能会阻止 通过促进卵泡生成，通过刺激黄体 功能，通过防止黄体溶解，或这些行动的组合。 具体来说，拟议的研究将检查孕酮是否 调节一些促进卵泡生成的参数，即 促性腺激素分泌，或卵巢对促性腺激素的反应，或两者兼而有之。 首先，我们将研究孕酮是否仅作用于卵巢。 随后的实验将研究孕酮是否能确保 通过调节FSH或脉冲式LH分泌来调节全长黄体期。 最后，探讨了孕酮促进 卵巢内的卵泡发生将通过测量其 对卵泡类固醇产生以及卵泡膜和颗粒细胞的影响 结合125 I-hCG。 技术包括：LH、FSH的放射免疫测定， 雌二醇、睾酮和孕酮;持续递送 通过渗透微型泵或硅橡胶植入物的激素;血液收集; 卵巢动脉插管; GnRH主动免疫; 卵巢切除术; GnRH激动剂可逆性终止周期;在 颗粒细胞的体外孵育，以及卵巢卵泡膜的测量 和颗粒细胞LH受体。 这些研究的结果应： (1)为我们了解神经内分泌机制提供了新的视角 控制发情周期及其开始和结束;（2） 增加我们对控制回收的机制的了解， 促性腺激素释放激素激动剂治疗后的周期性;（3）增加我们的 了解短黄体期的神经内分泌控制， 预防短黄体期不孕症;（4）提供我们 关于孕酮在促进 卵泡发生 最后，这些发现应该适用于 临床情况类似于 非周期性和周期性，如青春期、绝经期或 在用GnRH治疗性早熟或子宫内膜异位症后 促性腺激素释放激素激动剂，或使用促性腺激素释放激素激动剂作为避孕药。

The long-term goal of the proposed research is to elucidate the neuro- endocrine mechanisms whereby progesterone prevents short luteal phase cycles in ewes. It has been proposed that progesterone may prevent short luteal phases by promoting folliculogenesis, by stimulating luteal function, by preventing luteolysis, or a combination of these actions. Specifically, the proposed studies will examine whether progesterone modulates some of the parameters which promote folliculogenesis, namely gonadotropin secretion, or ovarian response to gonadotropins, or both. First, we will examine whether progesterone acts solely at the ovaries. Subsequent experiments will investigate whether progesterone ensures full-length luteal phases by modulating FSH or pulsatile LH secretion. Finally, the mechanism of action of progesterone in promoting folliculogenesis within the ovary will be investigated by measuring its effect on follicular steroid production and thecal and granulosa cell binding of 125I-hCG. Techniques include: radioimmunoassays for LH, FSH, estradiol, testosterone, and progesterone; sustained delivery of hormones via osmotic minipumps or Silastic implants; blood collection; cannulation of ovarian artery; active immunization against GnRH; ovariectomy; reversible termination of cycles with GnRH agonist; in vitro incubation of granulosa cells, ad measurement of ovarian thecal and granulosa cell LH receptors. The results of these studies should: (1) provide us with new insight into the neuroendocrine mechanisms controlling estrous cycles and their initiation and termination; (2) increase our knowledge of the mechanisms controlling recovery of cyclicity following treatment with GnRH agonist; (3) increase our understanding of the neuroendocrine control of short luteal phases and the prevention of short luteal phase infertility; and (4) provide us with new information regarding the role of progesterone in promoting folliculogenesis. Finally, these findings should be applicable to the clinical situations analogous to transitions between states of acyclicity and cyclicity, such as puberty, menopause, or those occurring following treatment of precocious puberty or endometriosis with GnRH agonists, or following use of GnRH agonists as contraceptives.