New insights into the control of pulsatile GnRH release: the role of Kiss1/neurokinin B neurons.
New insights into the control of pulsatile GnRH release: the role of Kiss1/neurokinin B neurons.
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DOI：
10.3389/fendo.2012.00048
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发表时间：
2012
影响因子：
5.2
通讯作者：
Navarro VM
中科院分区：
文献类型：
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作者：
Navarro VM
促性腺激素释放激素（GnRH）是神经内分泌因子复杂网络的最终输出信号，作用于垂体，触发促性腺激素释放。反过来，促性腺激素对性腺发挥其营养作用，刺激性类固醇的合成，从而通过GnRH释放的反馈调节机制完成促性腺轴。这些反馈循环在两种性别中都具有主要抑制作用，导致从青春期开始GnRH的紧张性脉冲式释放。然而，在女性中，雌二醇水平的上升沿着发情周期引起额外的正反馈，促使排卵前GnRH释放的激增模式。Kisspeptins，分泌的下丘脑Kiss 1神经元，准备作为主要管道，以调节这一双重分泌途径。Kiss1神经元在起源、性质和功能上是多样的，在两个主要的下丘脑核团中召集不同的神经元群体：弓状核（ARC）和前腹侧室周核。我们小组和其他人最近的研究指出，ARC中的Kiss 1神经元是GnRH脉冲的合理发生器，通过由Kiss 1神经元（所谓的KNDy神经元）中共同表达的神经激肽B（NKB）和强啡肽A（Dyn）的协调作用形成的脉冲式kisspeptin释放系统。在这篇综述中，我们的目的是记录最近的研究结果和工作模型，通过对该领域的最新技术的概要概述，确定GnRH释放的Kiss1依赖机制。
Gonadotropin-releasing hormone (GnRH) is the ultimate output signal of an intricate network of neuroendocrine factors that, acting on the pituitary, trigger gonadotropin release. In turn, gonadotropins exert their trophic action on the gonads to stimulate the synthesis of sex steroids thus completing the gonadotropic axis through feedback regulatory mechanisms of GnRH release. These feedback loops are predominantly inhibitory in both sexes, leading to tonic pulsatile release of GnRH from puberty onward. However, in the female, rising levels of estradiol along the estrous cycle evoke an additional positive feedback that prompts a surge-like pattern of GnRH release prior to ovulation. Kisspeptins, secreted from hypothalamic Kiss1 neurons, are poised as major conduits to regulate this dual secretory pathway. Kiss1 neurons are diverse in origin, nature, and function, convening distinct neuronal populations in two main hypothalamic nuclei: the arcuate nucleus (ARC) and the anteroventral periventricular nucleus. Recent studies from our group and others point out Kiss1 neurons in the ARC as the plausible generator of GnRH pulses through a system of pulsatile kisspeptin release shaped by the coordinated action of neurokinin B (NKB) and dynorphin A (Dyn) that are co-expressed in Kiss1 neurons (so-called KNDy neurons). In this review, we aim to document the recent findings and working models directed toward the identification of the Kiss1-dependent mechanisms of GnRH release through a synoptic overview of the state-of-the-art in the field.