ERRα regulates synaptic transmission through reactive oxygen species in hippocampal neurons

作者全名："Xu, De-Mei; Zhang, Zhi-Juan; Guo, Hao-Kun; Chen, Guo-Jun; Ma, Yuan-Lin"

作者地址："[Xu, De-Mei; Zhang, Zhi-Juan; Guo, Hao-Kun; Chen, Guo-Jun; Ma, Yuan-Lin] Chongqing Med Univ, Affiliated Hosp 1, Dept Neurol, Chongqing Key Lab Neurol, 1 Youyi Rd, Chongqing 400016, Peoples R China"

通信作者："Chen, GJ; Ma, YL (通讯作者)，Chongqing Med Univ, Affiliated Hosp 1, Dept Neurol, Chongqing Key Lab Neurol, 1 Youyi Rd, Chongqing 400016, Peoples R China."

来源：HELIYON

ESI学科分类：　

WOS号：WOS:001147725000001

JCR分区：Q2

影响因子：4

年份：2024

卷号：10

期号：1

开始页：　

结束页：　

文献类型：Article

关键词：ERR alpha; ROS; Dendritic spines; Synaptic transmission; PBN

摘要："Reactive oxygen species (ROS) play multiple roles in synaptic transmission, and estrogen-related receptor alpha (ERR alpha) is involved in regulating ROS production. The purpose of our study was to explore the underlying effect of ERR alpha on ROS production, neurite formation and synaptic transmission. Our results revealed that knocking down ERR alpha expression affected the formation of neuronal neurites and dendritic spines, which are the basic structures of synaptic transmission and play important roles in learning, memory and neuronal plasticity; moreover, the amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) were decreased. These abnormalities were reversed by overexpression of human ERR alpha. Additionally, we also found that knocking down ERR alpha expression increased intracellular ROS levels in neurons. ROS inhibitor PBN rescued the changes in neurite formation and synaptic transmission induced by ERR alpha knockdown. These results indicate a new possible cellular mechanism by which ERR alpha affects intracellular ROS levels, which in turn regulate neurite and dendritic spine formation and synaptic transmission."

基金机构："National Natural Science Foundation of China [:82101517, 81901332]"

基金资助正文："<B>Funding</B> This work was supported by the National Natural Science Foundation of China (grant numbers:82101517, 81901332) ."