Estradiol requirements for induction and maintenance of the gonadotropin-releasing hormone surge: Implications for neuroendocrine processing of the estradiol signal
Estradiol requirements for induction and maintenance of the gonadotropin-releasing hormone surge: Implications for neuroendocrine processing of the estradiol signal
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DOI：
10.1210/en.138.12.5408
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发表时间：
1997-12-01
期刊：
影响因子：
4.8
通讯作者：
Karsch, FJ
中科院分区：
文献类型：
--
作者：
Evans, NP;Dahl, GE;Karsch, FJ
进行了两项实验来检查雌二醇信号对母羊 GnRH 和 LH 激增的时间要求。从人工卵泡期模型中建立的母羊身上采集垂体门静脉血和颈静脉血（分别测量 GnRH 和 LH）。撤回黄体酮以模拟黄体溶解后，通过插入雌二醇植入物将循环雌二醇升高至排卵前水平，然后在不同时间将其移除以改变雌二醇信号持续时间。第一个实验的目的是评估在激增开始时撤回雌二醇对 GnRH/LH 激增的发展和维持的影响。在激增发生之前去除雌二醇，既不会改变与维持雌二醇刺激时诱导的 LH 激增相关的情况，也不会影响对比 LH 激增持续数小时的大规模且持续的 GnRH 激增的刺激。然而，持续的雌二醇治疗确实延长了 GnRH 的峰值。在第二个实验中，缩短了雌二醇刺激时间，以检验这样的假设：雌二醇不需要在整个前波峰期间存在来诱导 GnRH/LH 波峰。母羊在浪涌开始时（21 小时）或相当于 21 小时信号的最后 14 小时、最后 7 小时或最早 7 小时的时间段内接受雌二醇。将信号缩短至 14 小时并不会降低其刺激完全 GnRH 激增的能力，但确实降低了由此产生的 LH 激增的幅度。然而，将信号进一步缩短至 7 小时，会产生不同的反应。大多数动物（两个 7 小时组的 10 只动物中的 8 只）不表达 GnRH 激增。在这样做的两只母羊中，GnRH 激增幅度和持续时间再次处于 21 小时雌二醇信号观察到的范围内，但 LH 响应大大降低。这些结果表明，一旦母羊的 GnRH/LH 激增开始，不需要升高雌二醇来维持激增。完全 GnRH 激增的发生仅需要在激增前的一部分时间内升高雌二醇。然而，需要更长时间地接触雌二醇才能最大限度地提高垂体对 GnRH 的反应。由于 GnRH 激增的雌二醇信号相对较短（7-14 小时），并且在时间上位于激增本身之前，因此这些结果与以下假设一致：雌二醇仅需要激活类固醇反应性神经元元件，而不需要将信号从这些元件进展到 GnRH 释放的实际激增过程。
Two experiments were performed to examine the temporal requirements of the estradiol signal for the GnRH and LH surges in the ewe. Hypophyseal portal and jugular blood (to measure GnRH and LH, respectively) were sampled from ewes set up in an artificial follicular phase model. After progesterone withdrawal to simulate luteolysis, circulating estradiol was raised to a preovulatory level by inserting estradiol implants, which then were removed at different times to vary estradiol signal duration. The objective of the first experiment was to assess the effect of withdrawing estradiol at surge onset on development and maintenance of the GnRH/LH surges. Removal of estradiol, before surge onset, neither altered the LH surge in relation to that induced when the estradiol stimulus was maintained nor affected stimulation of a massive and sustained GnRH surge that outlasted the LH surge by many hours. Continued estradiol treatment, however, did prolong the GnRH surge. In the second experiment, the estradiol stimulus was shortened to test the hypothesis that estradiol need not be present for the whole presurge period to induce GnRH/LH surges. Ewes received estradiol either up to the time of surge onset (21 h) or for periods equivalent to the last 14 h, the last 7 h, or the earliest 7 h of the 21-h signal. Shortening the signal to 14 h did not reduce its ability to stimulate a full GnRH surge, but it did reduce the amplitude of the resultant LH surge. Further shortening of the signal to 7 h, however, produced a mixed response. Most animals (8 of 10 combining the two 7-h groups) did not express GnRH surges. In the two ewes that did, GnRH surge amplitude and duration were again within the range observed with the 21-h estradiol signal, but the LH response was greatly reduced.These results indicate that, once the GnRH/LH surges of the ewe have begun, elevated estradiol is not required for surge maintenance. Development of a full GnRH surge requires elevated estradiol for only a portion of the presurge period. More prolonged exposure to estradiol, however, is needed to maximize pituitary responsiveness to GnRH. Since the estradiol signal for the GnRH surge is relatively short (7-14 h) and temporally located well in advance of the surge itself, these results are consistent with the hypothesis that estradiol is required only to activate the steroid-responsive neuronal elements and not for progression of the signal from these elements to the actual surge process of GnRH release.