如何控制早发促黄体生成素（LH）峰是超促排卵的核心问题。我们团队提出以孕激素抑制自发排卵为理念的超排卵方案通过在下丘脑水平抑制LH峰，临床上已证明更加安全高效，但神经机理尚未明确。LH峰的发生以LH脉冲频率的增加为前提，受到AVPV和ARC核团的协同调控。我们前期已证实孕激素抑制LH峰的作用靶点是AVPV核团kisspeptin神经元，而ARC核团投射Glutamate到AVPV核团，通过kisspeptin神经元参与对LH峰的调控。因此我们提出假说:孕激素可能通过减少ARC向AVPV核团kisspeptin神经元释放兴奋性神经递质Glutamate来抑制LH峰的形成。本项目在已建立的光遗传模型基础上结合药理学、电生理学和免疫组化等实验证Glutamate神经通路在孕激素抑制LH峰中的调控作用，并明确其上下游调控因子。本研究将阐述LH峰抑制的神经机制，为优化促排卵中关键步骤提供科学依据。

How to control premature LH surge is essential to controlled ovarian hyperstimulation. Our research team has found that the application of progesterone to suppress premature LH surge in controlled ovarian hyperstimulation is effective and efficient. Progesterone block LH surge by relying on the feedback loop of the hypothalamus, while the related neural mechanism is still largely unknown. The occurrence of LH surge is premised on the increase of LH pulse frequency, which is coordinated by AVPV and ARC nucleus. Our previous research has confirmed that the AVPV nucleus kisspeptin neuron is the target of progesterone's inhibition on LH surge and the ARC nucleus participates in the regulation of the LH surge through projecting Glutamate to this target. Therefore, our hypothesis is that progesterone may inhibit the formation of LH surge by reducing the release of excitatory neurotransmitter Glutamate from ARC to kisspeptin neurons of AVPV nucleus. Based on the established optogenetic model, our project combines pharmacology, electrophysiology and immunohistochemistry to verify the regulatory role of Glutamate neural pathway in the inhibition of progesterone on LH surge, and clarify its upstream and downstream regulatory factors. This project will elaborate the neural mechanism of LH surge inhibition and provide scientific evidence for the optimization of key steps in ovulation stimulation.