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首页> 美国卫生研究院文献>Endocrinology >Developmental GnRH Signaling Is Not Required for Sexual Differentiation of Kisspeptin Neurons but Is Needed for Maximal Kiss1 Gene Expression in Adult Females
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Developmental GnRH Signaling Is Not Required for Sexual Differentiation of Kisspeptin Neurons but Is Needed for Maximal Kiss1 Gene Expression in Adult Females

机译：Kisspeptin神经元的性别分化不需要发育GnRH信号但成年女性最大的Kiss1基因表达是必需的

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摘要

Kisspeptin, encoded by Kiss1, stimulates reproduction. In rodents, one Kiss1 population resides in the hypothalamic anterior ventral periventricular nucleus and neighboring rostral periventricular nucleus (AVPV/PeN). AVPV/PeN Kiss1 neurons are sexually dimorphic (greater in females), yet the mechanisms regulating their development and sexual differentiation remain poorly understood. Neonatal estradiol (E2) normally defeminizes AVPV/PeN kisspeptin neurons, but emerging evidence suggests that developmental E2 may also influence feminization of kisspeptin, although exactly when in development this process occurs is unknown. In addition, the obligatory role of GnRH signaling in governing sexual differentiation of Kiss1 or other sexually dimorphic traits remains untested. Here, we assessed whether AVPV/PeN Kiss1 expression is permanently impaired in adult hpg (no GnRH or E2) or C57BL6 mice under different E2 removal or replacement paradigms. We determined that 1) despite lacking GnRH signaling in development, marked sexual differentiation of Kiss1 still occurs in hpg mice; 2) adult hpg females, who lack lifetime GnRH and E2 exposure, have reduced AVPV/PeN Kiss1 expression compared to wild-type females, even after chronic adulthood E2 treatment; 3) E2 exposure to hpg females during the pubertal period does not rescue their submaximal adult Kiss1 levels; and 4) in C57BL6 females, removal of ovarian E2 before the pubertal or juvenile periods does not impair feminization and maximal adult AVPV/PeN Kiss1 expression nor the ability to generate LH surges, indicating that puberty is not a critical period for Kiss1 development. Thus, sexual differentiation still occurs without GnRH, but GnRH or downstream E2 signaling is needed sometime before juvenile development for complete feminization and maximal Kiss1 expression in adult females.
机译：由Kiss1编码的Kisspeptin刺激繁殖。在啮齿动物中，一个Kiss1种群居住在下丘脑前腹侧室旁核和邻近的喙状室旁核（AVPV / PeN）中。 AVPV / PeN Kiss1神经元具有性二态性（女性更大），但调节其发育和性别分化的机制仍知之甚少。新生儿雌二醇（E2）通常会使AVPV / PeN Kisspeptin神经元脱女性化，但是新兴证据表明，发育E2也可能影响Kisspeptin的女性化作用，尽管尚不清楚该过程何时发生。此外，GnRH信号在控制Kiss1的性别分化或其他性二形性特征中的强制性作用尚未得到检验。在这里，我们评估了在不同的E2去除或替代模式下，成年hpg（无GnRH或E2）或C57BL6小鼠的AVPV / PeN Kiss1表达是否永久受损。我们确定1）尽管在发育中缺乏GnRH信号传导，但hpg小鼠中Kiss1仍存在明显的性别分化； 2）即使在长期成年E2治疗后，缺乏终生GnRH和E2暴露的成年hpg雌性与野生型雌性相比，AVPV / PeN Kiss1表达也降低。 3）在青春期，hPG雌性的E2暴露不能挽救其​​成年Kiss1水平的最大水平；和4）在C57BL6女性中，在青春期或少年期之前去除卵巢E2不会损害女性化和最大的成年AVPV / PeN Kiss1表达，也不会产生LH激增的能力，这表明青春期不是Kiss1发育的关键时期。因此，在没有GnRH的情况下仍会发生性别分化，但是在成年女性发育完全女性化和最大Kiss1表达之前，需要GnRH或下游E2信号传导。

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