NEUROENDOCRINE REGULATION OF OVINE ESTROUS CYCLES

这项拟议研究的长期目标是阐明神经- 孕酮阻止黄体期缩短的内分泌机制 在母羊身上循环。有人提出，黄体酮可能会阻止 通过促进卵泡发生和刺激黄体来缩短黄体期 功能，通过防止黄体溶解，或这些作用的组合。 具体地说，拟议的研究将检查黄体酮 调节一些促进卵泡发生的参数，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，我们将检查黄体酮是否只作用于卵巢。 随后的实验将调查黄体酮是否能确保 通过调节卵泡刺激素或搏动性黄体生成素分泌的全长黄体期。 黄体酮促黄体生成素的作用机制 卵巢内的卵泡发生将通过测量其 对卵泡类固醇分泌和卵泡膜颗粒细胞的影响 结合~(125)I-hCG。技术包括：黄体生成素、卵泡刺激素、 雌二醇、睾酮和黄体酮；持续给药 通过渗透性微泵或硅橡胶植入的激素；采血； 卵巢动脉插管；促性腺激素释放激素主动免疫； 卵巢切除；用促性腺激素释放激素激动剂可逆性终止周期 颗粒细胞的体外培养及卵泡膜厚度的测定 颗粒细胞的黄体生成素受体。这些研究的结果应该是： (1)为我们提供了对神经内分泌机制的新见解 控制发情周期及其启动和终止；(2) 增加我们对控制恢复的机制的了解 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 对黄体短时和黄体功能障碍的神经内分泌调控的认识 预防黄体期过短不孕症；及(4)为我们提供 关于孕酮在促性腺激素中作用的新信息 卵泡发生。最后，这些发现应该适用于 类似于状态转换的临床情况 无周期性和周期性，如青春期、更年期或发生的 促性腺激素释放激素治疗性早熟或子宫内膜异位症 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.