GONADOTROPIN REGULATION AND REPRODUCTION IN THE MALE

尽管众所周知，慢性肾上腺皮质激活会 抑制啮齿动物的生殖功能，关于 促肾上腺皮质激素(ACTH)的精确作用 下丘脑-垂体-睾丸轴。这篇文章中概述的研究 提案将继续我们对肾上腺-性腺相互作用的研究 在男性中，也检查了成人服用ACTH的效果 就像刚出生的男性一样。在各种物种中进行的研究，包括 男人，已经表明慢性ACTH治疗会抑制血浆 睾丸激素水平。相比之下，为数不多的几项调查研究 ACTH对男性的急性影响观察到在 循环中的睾丸素。将进行实验，以检验这两个 控制注射ACTH对雄性大鼠的急性和慢性影响。 下丘脑LHRH含量和垂体反应性的测定 在这些实验中使用外源性LHRH，利用 完整的、去势的、接受睾丸激素治疗的雄性应该提供 有关ACTH对成人下丘脑和垂体影响的信息。 此外，ACTH对睾丸血流和对 将对HCG刺激进行研究，以评估 肾上腺皮质激活对睾丸功能的影响。在新生儿男性中，我们 此前已有研究表明，ACTH治疗3天会导致持续的 在不影响血浆促黄体生成素的情况下降低循环中的促卵泡刺激素滴度 浓度。ACTH的这种作用显然不是通过 促进皮质酮分泌，但至少部分可以通过以下方式模仿 出生后晚期(第7天至第9天)雄激素注射。研究将会是 以确定哪种雄激素参与了这种反应，并 评估下丘脑和垂体控制的可能变化。 促性腺激素分泌。下丘脑LHRH含量及分布，AS 以及流向大脑不同区域的血液也将在 表现出促性腺激素调节变化的动物(即早期和 新生儿晚期雄激素化的男性和长期阉割的男性)。这些 实验将评估不同LHRH途径的相对重要性 在调节脑垂体卵泡刺激素和黄体生成素的分泌，并将提供 下丘脑血流在促性腺激素中作用的研究进展 监管。

Although it is well known that chronic adrenocortical activation will suppress reproductive function in rodents, little information exists on the precise actions of adrenocorticotropic hormone (ACTH) on the hypothalamic-pituitary-testicular axis. The studies outlined in this proposal will continue our investigations of adrenal-gonadal interactions in the male, examining the effects of ACTH administration in adult as well as in neonatal males. Studies conducted in a variety of species, including man, have shown that chronic ACTH treatment will suppress plasma testosterone levels. In contrast, the few studies which have investigated acute effects of ACTH administration to males have observed an elevation in circulating testosterone. Experiments will be conducted to examine both acute and chronic effects of controlled ACTH infusions in male rats. Measurements of hypothalamic LHRH content and the pituitary responsiveness to exogenous LHRH administration in these experiments, utilizing both intact and castrated, testosterone-treated males, should provide information about hypothalamic and pituitary effects of ACTH in the adult. In addition, effects of ACTH on testicular blood flow and responsiveness to hCG stimulation will be studied in order to evaluate effects of adrenocortical activation on testicular function. In neonatal males, we have previously shown that ACTH treatment for 3 days induced a persistent reduction in circulating FSH titers while not affecting plasma LH concentrations. This effect of ACTH is apparently not mediated via enhanced corticosterone secretion but can be mimicked, at least in part, by late postnatal (day 7 to 9) androgen administration. Studies will be conducted to determine which androgen is involved in this response and to evaluate possible alterations in the hypothalamic and pituitary control of gonadotropin secretion. Hypothalamic LHRH content and distribution, as well as blood flow to various regions of the brain will also be studied in animals showing alterations in gonadotropin regulation (i.e. early- and late- neonatally androgenized males and long-term castrated males). These experiments will evaluate the relative importance of various LHRH pathways in the regulation of pituitary FSH and LH secretion and will provide information about the role of hypothalamic blood flow in gonadotropin regulation.