PROGESTERONE MODULATION OF GONADOTROPIN-SECRETION BY DISPERSED RAT PITUITARY-CELLS IN CULTURE .1. BASAL AND GONADOTROPIN-RELEASING HORMONE-STIMULATED LUTEINIZING-HORMONE RELEASE

PROGESTERONE MODULATION OF GONADOTROPIN-SECRETION BY DISPERSED RAT PITUITARY-CELLS IN CULTURE .1. BASAL AND GONADOTROPIN-RELEASING HORMONE-STIMULATED LUTEINIZING-HORMONE RELEASE
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DOI:
10.1016/0303-7207(90)90180-g
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发表时间:
1990-01-22
影响因子:
4.1
通讯作者:
KAMEL, F
KAMEL, F
中科院分区:
医学2区
文献类型:
--
作者:
KREY, LC;KAMEL, F

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培养分散的、经雌二醇处理的大鼠垂体细胞,研究生理浓度的孕酮(P,10-7M)对促性腺激素释放激素(GnRH)反应性的影响。急性(<6h)P处理增强和慢性(>12h)处理抑制基础和GnRH刺激的黄体生成素(LH)释放。这种调节发生在细胞内的黄体生成素储存量没有任何变化的情况下,这表明分泌的变化不是由于黄体生成素合成的变化,也不伴随基础或TRH刺激的催乳素分泌的类似变化。此外,这些反应的时间是固定的,因为低10倍的磷浓度只会导致黄体生成素释放的更小和更短暂的变化。对有效P刺激的时间特征的分析表明,短暂的P暴露6h可抑制18h后GnRH刺激的促黄体生成素分泌。与之相反,P‘’S的急性作用在从培养液中去除类固醇后迅速消失。最后,P对促性腺激素释放激素刺激的促黄体生成素释放的增强和抑制可以被适当时机的蛋白质合成抑制剂所阻断。我们的发现与P通过产生特定蛋白质影响促性腺激素分泌功能的假说是一致的。
Dispersed, estradiol-treated, rat pituitary cells were cultured to characterize the influences of a physiologic concentration of progesterone (P, 10-7 M) on gonadotroph responsiveness to gonadotropin-releasing hormone (GnRH). Acute (< 6 h) P treatment enhanced and chronic (> 12 h) treatment suppressed both basal and GnRH-stimulated luteinizing hormone (LH) release. This modulation took place without any change in intracellular LH stores, indicating that the secretory changes are not attributable to changes in LH synthesis, and were not accompanied by similar alterations in basal or TRH-stimulated prolactin secretion. Moreover, the timing of these responses was fixed since a 10-fold lower P concentration produced only smaller and briefer alterations in LH release. Analyses of the temporal characteristics of effective P stimuli indicated that a brief 6 h exposure to P inhibited GnRH-stimulated LH secretion 18 h later. In contrast, P''s acute actions rapidly dissipated following removal of the steroid from the culture medium. Finally, P-induced enhancement and suppression of GnRH-stimulated LH release could be blocked by appropriately timed treatments with protein synthesis inhibitors. Our findings are consistent with the hypothesis that P influences gonadotroph secretory function via the production of specific proteins.