由HCN1高极化激活的循环核酸通道增强了来自帕瓦胺阳性内部神经元的唤起的GABA释放
Eric W Buss1, Olivia M Lofaro1, Anastasia Barnett1
1Departments of Neuroscience and Pharmacology, Kavli Institute for Brain Science, Zuckerman Mind Brain Behavior Institute, Columbia University Medical Center, New York, NY 10027.
概括
在抑制性内部神经元中,高极化激活的循环核酸通道1 (HCN1) 促进了海马中GABA的释放. 阻断HCN1减少CA1金字塔神经元中的抑制后突触电流.
科学领域:
- 神经科学是一个神经科学.
- 分子和细胞生物学分子和细胞生物学
背景情况:
- 超极化激活的循环核酸门 (HCN) 通道,特别是HCN1,对于神经元刺激性至关重要.
- 在海马区CA1中发现了HCN1通道,包括帕瓦胺阳性内部神经元 (PV+INs) 的前突触终端.
- 在调节从PV+IN前突触终端释放GABA的过程中,HCN1的作用在很大程度上仍未被探索.
研究的目的:
- 研究PV+IN中HCN1通道的功能.
- 为了确定HCN1在前突触终端的活动如何影响GABA释放到CA1金字塔神经元 (PNs).
- 阐明HCN1对PV+IN电生理特性及其后的突触传播的影响.
主要方法:
- 基因操纵 (HCN1淘汰赛小鼠).
- 选择性PV+IN刺激的光遗传学.
- 电生理学 (IPSCs,电流).
- 预突触Ca2+动态的双光子成像.
主要成果:
- 药理学阻断HCN1降低了CA1PNS中的抑制后突触潜能 (IPSP) 幅度.
- HCN1淘汰赛小鼠表现出抑制后突触电流 (IPSCs) 的减少.
- 在刺激时,HCN1阻断剂降低了PV+IN前突触中Ca2+过渡体的概率.
结论:
- 在PV+内部神经元的轴突末端的HCN1通道促进GABAergic传递.
- 在前突触终端中的HCN1活性对于调节海马体CA1区域的GABA释放至关重要.
- 这些发现强调了HCN1在调节抑制性神经传递中的新作用.
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