Activation of estradiol-positive feedback at puberty: estradiol sensitizes the LHRH-releasing system at two different biochemical steps.
Activation of estradiol-positive feedback at puberty: estradiol sensitizes the LHRH-releasing system at two different biochemical steps.
复制标题
青春期雌二醇正反馈的激活：雌二醇在两个不同的生化步骤中使 LHRH 释放系统变得敏感。
DOI：
10.1159/000124535
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发表时间：
1986
影响因子：
4.1
通讯作者：
Costa,ME
中科院分区：
文献类型：
--
作者：
Ojeda,SR;Urbanski,HF;Katz,KH;Costa,ME
为探讨雌二醇(E_2)是否能影响雌性大鼠青春期开始时促黄体激素释放激素(LHRH)释放的某些神经细胞内机制。正中隆起(ME)神经末梢分泌LHRH的能力在幼年-青春期早期(出生后22-34天)显著增加，这取决于它们的基础LHRH释放和体外对前列腺素E_2(PGE_2)的反应。第22天卵巢切除(OVX)导致第34天LHRH对PGE2的反应显著降低。E2通过S.C.硅胶胶囊在复制青少年血清E2水平的剂量下，恢复了这种反应。模拟幼年晚期(28日龄)雌性大鼠第一次发情时的血清E2水平，增强了含LHRH的终末对PGE2的敏感性和反应性。此外，E2增强LHRH终末对去甲肾上腺素(NE)的敏感性和反应性。这种效应似乎与LHRH对PGE2的反应增加和PGE2合成途径对NE的敏感性增加有关。这是因为雌二醇组大鼠的MES对去甲肾上腺素浓度的反应显着增加了PGE2的释放，而在未经处理的对照组中几乎不起作用。结果提示，雌鼠首次排卵前释放LHRH的机制之一是通过促进两种不同但顺序相关的生化事件的发生：NE刺激PGE2的形成和PGE2促进LHRH的释放。此外，LHRH对PGE2的反应性的维持似乎是E=依赖性的，PGE2被认为是NE诱导的LHRH释放的必备成分。
Experiments were performed to examine whether estradiol (E2) can influence some of the intraneuronal mechanisms involved in luteinizing hormone-releasing hormone (LHRH) release during the onset of puberty in the female rat. The capacity of median eminence (ME) nerve terminals to secrete LHRH, as determined by both their basal release of LHRH and by their response to prostaglandin E2(PGE2) in vitro, increased significantly during the juvenile-early peripubertal periods of development (postnatal days 22–34). Ovariectomy (OVX) on day 22 led to a striking reduction in LHRH response to PGE2 on day 34. E2administered via s.c. Silastic capsules, at a dose that reproduces juvenile serum E2levels, restored the response. Simulation of first proestrous serum E2 levels in late juvenile (28-day-old) female rats enhanced both the sensitivity and the responsivenes of LHRH-containing terminals to PGE2. Furthermore, E2enhanced the sensitivity and the responsiveness of LHRH terminals to norepinephrine (NE). This effect appeared to be related to both the increased LHRH response to PGE2and an enhanced sensitivity of the PGE2-synthesizing pathway to NE. This is because MEs from E2-treated rats showed a marked increase in PGE2release in response to a NE concentration which was barely effective in untreated controls. It is suggested that one of the mechanisms by which E2activates the first preovulatory discharge of LHRH release in the female rat is by facilitating the occurrence of two different but sequentially related biochemical events: the stimulation of PGE2formation by NE and the enhancement of LHRH release by PGE2. In addition, it appears that maintenance of LHRH responsiveness to PGE2, which has been implicated as an obligatory component of NE-induced LHRH release, is E=-dependent.