Alpha-synuclein promotes clathrin-mediated endocytosis of NMDA receptors in dopaminergic cells  

作　　者：Shun Yu 

机构地区：[1]Department of Neurobiology and the Sino-Japan Joint Laboratory on Neurodegenerative Diseases, Key Laboratory of NeurodegenerativeDiseases Capital Medical University, Ministry of Education, XuanwuHospital of China Capital Medical University, 100053 Beijing, China [2]UCLA-Kern Psychiatry Program and Kern County Mental Health, Bakersfield, California, USA

出　　处：《中国药理通讯》2012年第3期30-31,共2页

摘　　要：Loss of dopaminergic i a compensatory increase in nput to the striatum associated with Parkinson＇ s disease brings about glutamate release onto the dopaminergic cell bodies in the substantia nigra pars compacta （SNpc）[1] Glutamate over-activation of NMDA receptors on these cells can cause excitotoxicity and contribute to their further loss. NMDA receptor-mediated neuronal death is reduced by group I mGluR-mediated up-regulation of endocytosis protein RAB5B[2.3] Among proteins shown to interact with RAB5 proteins isLoss of dopaminergic i a compensatory increase in nput to the striatum associated with Parkinson＇ s disease brings about glutamate release onto the dopaminergic cell bodies in the substantia nigra pars compacta （SNpc）[1] Glutamate over-activation of NMDA receptors on these cells can cause excitotoxicity and contribute to their further loss. NMDA receptor-mediated neuronal death is reduced by group I mGluR-mediated up-regulation of endocytosis protein RAB5B[2.3] Among proteins shown to interact with RAB5 proteins is a-synuclein

关 键 词：TTP HSC SOD 药理学 NMDA 

分 类 号：R95[医药卫生—药学]