敏感于CCK的C纤维通过NMDA受体激活NTS瘦素受体表达神经元
Drew M Neyens1, Lynne Brenner1, Rowan Calkins1
1Department of Integrated Physiology and Neuroscience, Washington State University, Pullman, Washington, United States.
概括
大脑干中的勒素敏感神经元通过阴道神经从肠道接收信号. 胆囊托基宁 (CCK) 激活这些神经元,影响食物摄入量和体重调节.
科学领域:
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
- 胃肠病学 胃肠病学
背景情况:
- 素是一种激素,通过作用于中枢神经系统,包括孤独管 (NTS) 的核,调节食物摄入量和体重.
- 素受体 (lepRs) 存在于NTS神经元上,它们的功能对于调解素的厌食效应至关重要.
- 阴道腺体向NTS传输胃肠道信号,在食欲控制中发挥关键作用.
研究的目的:
- 描述NTS中素受体表达神经元 (lepR) 的阴道输入.
- 研究胆囊托基宁 (CCK) 和NMDA受体 (NMDARs) 在调节这些NTS神经元的活动中的作用.
主要方法:
- 在基因改造小鼠 (lepRCre × floxedTdTomato) 的脑切片中进行了全细胞记录.
- 使用电生理学技术来评估神经元对素,CCK和NMDAR激活的反应.
- 在体内实验中测量了c-fos表达,以确认外围CCK的神经元激活.
主要成果:
- NTS lepR神经元从对素敏感的C型阴道 afferents接收直接的单突触输入.
- 通过CCK受体 (CCKR1) 的介导,CCK刺激了勒普R神经元中的谷氨酸释放和动作潜力的激发.
- NMDARs有助于自发刺激后突触电流,并增强CCK诱导的神经元发射.
结论:
- 大多数NTS lepR神经元由CCK敏感的阴道 afferents直接内化.
- 外围和中央CCK都激活这些神经元,突出显示肠-大脑通信通路.
- 在NTS中,NMDARs在CCK介导的信号中发挥调节作用,影响食欲调节.
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