Electrophysiological phenotypes of synaptic transmission and neural network in hippocampal neurons of the α7-nAChR knockout mice.
- Author:
Chao ZHENG
1
;
Ling-Yun GAO
2
;
Huan-Huan ZHANG
2
;
Ying-Ying ZHA
2
;
Meng-Ya WANG
3
Author Information
1. Cell Electrophysiology Laboratory, Wannan Medical College, Wuhu 241002, China. chaozheng10@fudan.edu.cn.
2. Cell Electrophysiology Laboratory, Wannan Medical College, Wuhu 241002, China.
3. Cell Electrophysiology Laboratory, Wannan Medical College, Wuhu 241002, China. wangmy@wnmc.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Hippocampus;
cytology;
Mice;
Mice, Knockout;
Neurons;
physiology;
Phenotype;
Synaptic Transmission;
alpha7 Nicotinic Acetylcholine Receptor;
physiology
- From:
Acta Physiologica Sinica
2019;71(2):261-270
- CountryChina
- Language:English
-
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.
