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ATP11B deficiency leads to impairment of hippocampal synaptic plasticity

查看全文 作　　者：Jiao [1]Wang;Weihao [1]Li;Fangfang [1]Zhou;Ruili [1]Feng;Fushuai [1]Wang;Shibo [1]Zhang;Jie [1]Li;Qian [1]Li;Yajiang [1]Wang;Jiang [2]Xie;Tieqiao [1]Wen 高影响力作者 机构地区：[1]Laboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, Shanghai 200444, China;[2]School of Computer Engineering and Science, Shanghai University, Shanghai 200444, China高影响力机构 出　　处：《Journal of Molecular Cell Biology》索引2019年第11卷第8期,共15页高影响力期刊 基　　金：This work was supported bythe National Natural Science Foundation of China (31500827,81471162,and 61873156);Young Eastern Scholar (QD2015033);the Science and Technology Commission of Shanghai (14JC1402400);the Natural Science Foundation of Shanghai (17ZR1409900). 摘　　要：Synaptic plasticity is known to regulate and support signal transduction between neurons, while synaptic dysfunction contributes to multiple neurological and other brain disorders;however, the specific mechanism underlying this process remains unclear. In the present study, abnormal neural and dendritic morphology was observed in the hippocampus following knockout of Atpllb both in vitro and in vivo. Moreover, ATP11B modified synaptic ultrastructure and promoted spine remodeling via the asymmetrical distribution of phosphatidylserine and enhancement of glutamate release, glutamate receptor expression, and intracellular Ca^2+ concentration. Fuithermoe experimental results also indicate that ATP11B regulated synaptic plasticity in hippocampal neurons through the MAPK14 signaling pathway. In conclusion, our data shed light on the possible mechanisms underlying the regulation of synaptic plasticity and lay the foundation for the exploration of proteins involved in signal transduction during this process. 关 键 词：ATP11B SYNAPTIC plasticity GLUTAMATE RECEPTORS MAPK14 signaling pathway
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