PKCαphosphorylation of GLT-1 at Ser562/563 induces glutamate excitotoxicity in ischemia in mice  

作　　者：Yuqing Wang Jun Du Shanshan Lu Xia Li Yifei Chen Chao Yuan Sheng-Tao Hou Yizheng Wang 

机构地区：[1]The Brain Science Center,Beijing Institute of Basic Medical Sciences,100850 Beijing,China [2]Institute of Neuroscience,Chinese Academy of Sciences,200031 Shanghai,China [3]Brain Research Center and Department of Biology,Southern University of Science and Technology,1088 Xueyuan Blvd,Nanshan District,Shenzhen,518055 Guangdong Province,China [4]Huashan Hospital,Fudan University,Shanghai,China

出　　处：《Signal Transduction and Targeted Therapy》2022年第4期974-977,共4页信号转导与靶向治疗（英文）

基　　金：the National Natural Science Foundation of China(81830034);Shenzhen-Hong Kong Institute of Brain ScienceShenzhen Fundamental Research Institutions(2021SHIBS0002);Shenzhen Science and Technology Innovation Committee Research Grants(JCYJ20180504165806229,KQJSCX20180322151111754 to S.T.H.).

摘　　要：Dear Editor,Glutamate excitotoxicity due to its accumulation in the extracellular space is a major factor to the brain damage that occurs during the early stages of cerebral ischemia1.GLT-1 is mainly expressed in astrocytes,and it is responsible for almost 90%of glutamate uptake in the brain2.Although GLT-1 upregulation under the administration of ceftriaxone reduces ischemic brain damage,translational application of ceftriaxone in acute ischemia treatment is limited because several days are needed for the upregulation of GLT-1^(3),which misses the critical time window during which suppression of excitotoxicity will be effective.

关 键 词：ISCHEMIA PKCΑ damage CEREBRAL 

分 类 号：R74[医药卫生—神经病学与精神病学]