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α7烟碱型乙酰胆碱受体基因敲除小鼠海马神经元突触传递和神经网络的电生理表型

Electrophysiological phenotypes of synaptic transmission and neural network in hippocampal neurons of the α7-nAChR knockout mice.

作者信息

Zheng Chao, Gao Ling-Yun, Zhang Huan-Huan, Zha Ying-Ying, Wang Meng-Ya

机构信息

Cell Electrophysiology Laboratory, Wannan Medical College, Wuhu 241002, China.

出版信息

Sheng Li Xue Bao. 2019 Apr 25;71(2):261-270.

PMID:31008485
Abstract

It was reported that α7 nicotinic acetylcholine receptor (α7-nAChR) knockout (α7 KO) mice showed few functional phenotypes. The purpose of this study was to investigate the effect of α7 KO on the electrophysiological characteristics of hippocampus in mice. The effect of α7 KO on hippocampal CA3-CA1 synaptic transmission in mice was evaluated by standard extracellular field potential recordings. The electrophysiological phenotype of γ-aminobutyrate A receptors (GABA-Rs) of single hippocampal neuron was detected by perforated patch-clamp recordings. The results showed that, the slope of field excitatory postsynaptic potential (fEPSP) and carbachol-induced theta oscillation were significantly decreased in the hippocampal CA1 neurons of α7 KO mice, compared with those of wild type mice. Under the treatment of GABA-R agonist muscimol, the I-V curves of both the hippocampal CA1 and CA3 neurons of α7 KO mice shifted towards depolarizing direction obviously, compared with those of wild type mice. These results suggest that the hippocampal CA3-CA1 synaptic transmission in α7 KO mice was significantly impaired and GABA-R maturation was significantly delayed, indicating that the deletion of α7-nAChR gene could significantly change the electrophysiological function of the hippocampus. The results may provide a new understanding of the role of α7-nAChR in hippocampal function and associated diseases.

摘要

据报道,α7烟碱型乙酰胆碱受体(α7-nAChR)基因敲除(α7 KO)小鼠几乎没有功能性表型。本研究的目的是探讨α7 KO对小鼠海马体电生理特性的影响。通过标准细胞外场电位记录评估α7 KO对小鼠海马CA3-CA1突触传递的影响。采用穿孔膜片钳记录检测单个海马神经元γ-氨基丁酸A受体(GABA-Rs)的电生理表型。结果显示,与野生型小鼠相比,α7 KO小鼠海马CA1神经元的场兴奋性突触后电位(fEPSP)斜率和卡巴胆碱诱导的θ振荡显著降低。在GABA-R激动剂蝇蕈醇处理下,与野生型小鼠相比,α7 KO小鼠海马CA1和CA3神经元的I-V曲线明显向去极化方向移动。这些结果表明,α7 KO小鼠海马CA3-CA1突触传递明显受损,GABA-R成熟明显延迟,表明α7-nAChR基因缺失可显著改变海马体的电生理功能。该结果可能为α7-nAChR在海马体功能及相关疾病中的作用提供新的认识。

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