Ringstrom S J, Schwartz N B
Department of Natural Science, Loyola University of Chicago, IL 60626.
J Steroid Biochem. 1987;27(1-3):625-30. doi: 10.1016/0022-4731(87)90362-1.
Our previous work has suggested that glucocorticoid pretreatment suppresses the enhanced responsiveness to GnRH seen in serum LH 12 h after castration. By contrast, serum FSH continues to show the castration-induced hypersensitivity to GnRH. Our attempts to replicate this LH suppression in static pituitary culture in vitro were not successful. This suggested to us the possibility that corticoids in vivo might be preventing castration-induced increases in pituitary GnRH receptor levels. We tested this at 24 h post-castration and, in fact, corticoids did not suppress the increase in GnRH receptors. In addition to the aforementioned effects of corticoids, we have seen that cortisol reverses the castration-induced drop in pituitary FSH content. It does this for 7 days post-castration, even though it no longer has an effect in suppressing serum LH. Thus, our accumulated data reveal that glucocorticoids have a differential effect on LH and FSH synthesis and secretion. Further studies are needed to clarify the site(s) of action of glucocorticoids in gonadotropin secretion and synthesis. Glucocorticoids may well prove to be a key in unlocking the mystery of the mechanism of differential control of regulation of LH and FSH.
我们之前的研究表明，糖皮质激素预处理可抑制去势后12小时血清促黄体生成素（LH）中所见的对促性腺激素释放激素（GnRH）反应性的增强。相比之下，血清促卵泡生成素（FSH）持续显示出去势诱导的对GnRH的超敏反应。我们试图在体外静态垂体培养中复制这种LH抑制作用，但未成功。这使我们推测，体内的皮质激素可能会阻止去势诱导的垂体GnRH受体水平升高。我们在去势后24小时对此进行了测试，事实上，皮质激素并未抑制GnRH受体的增加。除了上述皮质激素的作用外，我们还发现皮质醇可逆转去势诱导的垂体FSH含量下降。在去势后7天内它都有此作用，即使它在抑制血清LH方面不再起作用。因此，我们积累的数据表明，糖皮质激素对LH和FSH的合成与分泌有不同的影响。需要进一步研究以阐明糖皮质激素在促性腺激素分泌和合成中的作用位点。糖皮质激素很可能被证明是解开LH和FSH调节差异控制机制之谜的关键。
