Multiple Mild Stimulations Reduce Membrane Distribution of CX3CR1 Promoted by Annexin al in Microglia to Attenuate Excessive Dendritic Spine Pruning and Cognitive Deficits Caused by a Transient Ischemic Attack in Mice

作     者：Lu Zheng Yi Wang Bin Shao Huijuan Zhou Xing Li Cai Zhang Ning Sun Jing Shi Lu Zheng;Yi Wang;Bin Shao;Huijuan Zhou;Xing Li;Cai Zhang;Ning Sun;Jing Shi

作者机构：Department of NeurobiologySchool of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Key Laboratory of Neurological DiseasesMinistry of EducationWuhan 430030China The Institute for Brain ResearchCollaborative Innovation and TechnologyWuhan 430030China Center for Brain ScienceHuazhong University of Science Department of Clinical LaboratoryThe First Affliated Hospital of Zhengzhou UniversityZhengzhou 450052China Department of ImmunologySchool of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China 

出 版 物：《Neuroscience Bulletin》 (神经科学通报（英文版）)

年 卷 期：2022年第38卷第7期

页      面：753-768页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基　　金：This work.was supported bythe National Natural Science Foundation of China(31771126) 

主　　题：Annexin al CX3CR1 Microglia Dendritic spine pruning Transient ischemic attack Multiple mild stimulations 

摘      要：A transient ischemic attack(TIA)can cause reversible and delayed impairment of cognition,but the specific mechanisms arestill *** al(ANXA1)is a phospholipid-binding ***,we confirmed that cognition and hippocampal synapses were impaired in TIA-treated mice,and this could be rescued by multiple mild stimulations(MMS).TIA promoted the interaction of ANXAl and CX3CR1,increased the membrane distribution of CX3CR1 in microglila,and thus enhanced the CX3CR1 and CX3CL1 *** phenomena induced by TIA could be reversed by ***,the CX3CR1 membrane distribution and CX3CR1-CX3CL1 interaction were upregulated in primary cultured microglia overexpressing ANXAl,and the spine density was significantly reduced in co-cultured microglia overexpressing ANXAl and ***,ANXAl overexpression in microglia abolished the protection of MMS after ***,our study provides a potential strategy for treating the delayed synaptic injury caused by TIA.