GnRH pulses--the regulators of human reproduction.
GnRH pulses--the regulators of human reproduction.
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发表时间：
1993
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通讯作者：
J. Marshall;A. Dalkin;D. Haisenleder;Marie L. Griffin;R. Kelch
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作者：
J. Marshall;A. Dalkin;D. Haisenleder;Marie L. Griffin;R. Kelch
本章回顾的数据提供了证据，表明GnRH分泌模式似乎是调节促性腺激素亚单位基因表达、促性腺激素合成和激素分泌的重要因素。促性腺激素合成的数据是在啮齿动物中获得的，因此，在应用于灵长类动物时必须谨慎解释。尽管有这种保留，数据表明在哺乳动物物种的调节机制的相似性。这些数据还提供了一个解释的机制，即一个单一的促性腺激素释放激素可以差异调节三个促性腺激素基因，并允许差异激素分泌。与这一观点总体一致，青春期成熟期间的观察结果显示，青春期GnRH脉冲式分泌增加，从促性腺激素分泌的FSH为主演变为促性腺激素分泌的LH为主。在男性中，GnRH的分泌模式在整个成年生活中似乎相当一致，但在女性中发生周期性变化，这可能对维持周期性排卵很重要。有人提出，一旦青春期成熟已经建立，GnRH分泌在一个相对较快的频率（每小时一个脉冲），重复排卵周期的一个基本特征是在黄体期减缓这种GnRH刺激：允许随后的优先FSH释放。这种GnRH分泌的减缓似乎受到雌二醇和孕酮的影响，它们的作用是增强下丘脑阿片活性。类似的机制，包括阿片张力增加，似乎与下丘脑性闭经和高泌乳素血症中观察到的频率降低和不规则GnRH刺激有因果关系。相反，某些形式的多囊卵巢疾病可能反映了雌二醇-孕酮/阿片类/GnRH神经元反馈机制的异常，未能建立青春期无排卵周期的减缓。由此产生的持续性GnRH刺激增加LH，从而导致卵泡成熟异常和卵巢雄激素产生增加。目前的数据支持这些假设，但未来的研究将确定这些观点是否正确。然而，目前的数据提供了强有力的支持，认为GnRH分泌的模式是一个关键因素，在调节差异促性腺激素的合成和分泌在哺乳动物物种。
The data reviewed in this chapter provide evidence that the pattern of GnRH secretion appears to be an important factor in regulating gonadotropin subunit gene expression, gonadotropin synthesis and hormone secretion. The data on gonadotropin synthesis were obtained in rodents and hence, must be interpreted with caution when applied to primates. Despite this reservation, the data suggest a similarity of regulatory mechanisms in mammalian species. The data also provide an explanation for the mechanisms whereby a single gonadotropin-releasing hormone can differentially regulate the three gonadotropin genes and allow differential hormone secretion. In overall agreement with this view, the observations during pubertal maturation reveal increasing GnRH pulsatile secretion during puberty with an evolution from predominant FSH to a predominant LH secretion by the gonadotropes. In males, the patterns of GnRH secretion appear to be fairly consistent throughout adult life, but in women cyclic changes occur which perhaps are important in maintaining cyclic ovulation. It is proposed that once pubertal maturation has been established, GnRH is secreted at a relatively fast frequency (one pulse per hour), and an essential feature of repeated ovulatory cycles is the slowing of this GnRH stimulus during the luteal phase: to allow subsequent preferential FSH release. This slowing of GnRH secretion appears to be effected by estradiol and progesterone acting to enhance hypothalamic opioid activity. Similar mechanisms involving increased opioid tone appear to be causally related to the reduced frequency and irregular GnRH stimulus seen in hypothalamic amenorrhea and hyperprolactinemia. In contrast, some forms of polycystic ovarian disease may reflect abnormalities of the estradiol-progesterone/opioid/GnRH neuron feedback mechanisms, with failure to establish slowing in the peripubertal anovulatory cycles. The resulting persistent GnRH stimulus increases LH with consequent effects of abnormal follicular maturation and enhanced ovarian androgen production. Present data are supportive of these hypotheses, but future studies will determine whether these views prove to be correct. However, current data provide strong support for the view that the pattern of GnRH secretion is a critical factor in the regulation of differential gonadotropin synthesis and secretion in mammalian species.