Relationship between Na + leak current channel in hippocampal dentate gyrus region and cognitive function in mice
10.3760/cma.j.cn131073.20220806.01210
- VernacularTitle:海马齿状回区钠离子渗漏通道蛋白与小鼠认知功能的关系
- Author:
Junbo ZHAO
1
;
Xiaoyuan GENG
;
Lijuan WANG
;
Xiaoyan ZHANG
;
Lihua JIANG
Author Information
1. 郑州大学第三附属医院麻醉科，郑州 450000
- Keywords:
Dentate gyrus;
Sodium channels;
Cognitive dysfunction
- From:
Chinese Journal of Anesthesiology
2022;42(12):1461-1464
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluate the relationship between Na + leak current channel (NALCN) in hippocampal dentate gyrus (DG) region and cognitive function in mice. Methods:Thirty-nine male wild type C57BL/6 mice, aged 6-8 weeks, weighing 18-22 g, were studied.Three mice were sacrificed to verify the expression of NALCN co-localized with neuronal nuclear antigen (NeuN) in the hippocampal DG region through immunofluorescence technique.The remaining 36 mice were divided into 2 groups ( n=18 each) by the random number table method: control group (group C) and NALCN gene knockout group (group KO). NALCN-shRNA virus was injected in hippocampal DG region in group KO, and scrambled-shRNA virus was injected in group C. Three weeks after virus injection, behavioral tests (Y maze test and open field test) were performed, then the animals were sacrificed, and the hippocampal tissues were removed for determination of the expression of NALCN protein and mRNA using Western blot and real-time polymerase chain reaction. Results:NALCN and NeuN colocalized a lot on the same neuron in the hippocampal DG region of mice, and NALCN was widely expressed in the hippocampal DG region.Compared with group C, the expression of NALCN protein and mRNA was significantly down-regulated, the times of entering the new arm were reduced, the duration of staying at the new arm was shortened ( P<0.05), and no significant change was found in the parameters mentioned above in the open field test in group KO ( P>0.05). Conclusions:NALCN in the hippocampal DG region is involved in the regulation of cognitive function in mice, and the down-regulation of NALCN may lead to cognitive decline.
