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雌激素依赖性的促性腺激素释放激素神经元谷氨酸能神经传递控制雌性动物的摄食回路。

Estrogenic-dependent glutamatergic neurotransmission from kisspeptin neurons governs feeding circuits in females.

机构信息

Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, United States.

Department of Biochemistry, Howard Hughes Medical Institute, University of Washington, Seattle, United States.

出版信息

Elife. 2018 Aug 6;7:e35656. doi: 10.7554/eLife.35656.

DOI:10.7554/eLife.35656
PMID:30079889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6103748/
Abstract

The neuropeptides tachykinin2 (Tac2) and kisspeptin (Kiss1) in hypothalamic arcuate nucleus Kiss1 (Kiss1) neurons are essential for pulsatile release of GnRH and reproduction. Since 17β-estradiol (E2) decreases mRNA expression in Kiss1 neurons, the role of Kiss1 neurons during E2-driven anorexigenic states and their coordination of POMC and NPY/AgRP feeding circuits have been largely ignored. Presently, we show that E2 augmented the excitability of Kiss1 neurons by amplifying mRNA expression and T-type calcium and h-currents. E2 increased mRNA expression and glutamatergic synaptic input to arcuate neurons, which excited POMC and inhibited NPY/AgRP neurons via metabotropic receptors. Deleting in Kiss1 neurons eliminated glutamate release and led to conditioned place preference for sucrose in E2-treated KO female mice. Therefore, the E2-driven increase in Kiss1 neuronal excitability and glutamate neurotransmission may play a key role in governing the motivational drive for palatable food in females.

摘要

下丘脑弓状核中的神经肽 Tac2（Tac2）和 Kiss1（Kiss1）神经元中的 kisspeptin（Kiss1）对于 GnRH 的脉冲释放和生殖至关重要。由于 17β-雌二醇（E2）降低了 Kiss1 神经元中的 mRNA 表达，因此 Kiss1 神经元在 E2 驱动的厌食状态及其协调 POMC 和 NPY/AgRP 摄食回路中的作用在很大程度上被忽视了。目前，我们发现 E2 通过放大 mRNA 表达和 T 型钙和 h 电流来增强 Kiss1 神经元的兴奋性。E2 增加了 mRNA 表达和弓状神经元的谷氨酸能突触输入，通过代谢型受体兴奋 POMC 并抑制 NPY/AgRP 神经元。在 Kiss1 神经元中删除 消除了谷氨酸释放，并导致 E2 处理的 KO 雌性小鼠对蔗糖产生条件性位置偏好。因此，E2 驱动的 Kiss1 神经元兴奋性和谷氨酸能神经传递的增加可能在调节女性对美味食物的动机驱动中发挥关键作用。

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