α-突触核蛋白促进多巴胺能神经细胞表面NMDA受体的内在化  

Alpha-synuclein Promotes Internalization of Surface N-methyl-D-aspartate Receptors in Dopaminergic Neuronal Cells

作　　者：程芙蓉[1] 李昕[1] 李尧华[1] 王玉兰[2] 张燕莉[1] 于顺[1] 

机构地区：[1]首都医科大学宣武医院神经生物学研究室神经变性病教育部重点实验室 [2]首都医科大学宣武医院中心实验室

出　　处：《首都医科大学学报》2010年第6期737-741,共5页Journal of Capital Medical University

基　　金：国家高技术研究发展计划( 863计划)重大项目(2006AA02A408);国家重点基础研究发展计划(973计划)重大项目(2011CB504100);国家自然科学基金(30270482;30271437;30430280;81071014);北京市自然科学基金(7022011;7102076);北京市属高等学校人才强教计划资助项目(PHR200907113)~~

摘　　要：目的研究α-突触核蛋白(α-synuclein,α-Syn)对多巴胺能神经细胞表面N-甲基-D-天门冬氨酸(N-methyl-D-aspartate,NMDA)受体的影响及其机制。方法免疫荧光标记法和Western blotting分析法测定NMDA受体(NMDAR)和Rab5b含量。低钾休克抑制内吞,Rab5b反义寡核苷酸抑制Rab5b基因表达。以MES23.5多巴胺能神经细胞为模型,观察细胞外添加α-Syn蛋白对细胞膜NMDAR含量的影响以及内吞和Rab5b的作用。结果α-Syn(10μmol/L)明显上调Rab5b表达,下调细胞表面NMDAR;低钾休克及抑制Rab5b表达可消除α-Syn的这一作用。结论α-Syn通过上调Rab5b的表达促进NMDAR的内在化。Objective To investigate the effect of α-synuclein（α-Syn） on surface N-methyl-D-aspartate（NMDA） receptors.Methods Immunofluorescent labeling and western blotting analysis were used to measure the alterations of NMDA receptors and Rab5b proteins.Hypotonic K＋ shock was used to inhibit the internalization process.Rab5b antisense oligonucleotides were applied to suppress Rab5b expression.The MES 23.5 dopaminergic cells were used as model cells to observe the effect of α-Syn on the surface NR1 expression.Results Treatment of MES23.5 cultures with 10 μmol/L of α-Syn triggered a significant decrease of the surface NR1 expression.This effect of of α-Syn was blocked by hypotonic K＋ shock and suppression of Rab5b expression.Conclusion α-Syn promotes internalization of surface NMDA receptors by increasing Rab5b expression.

关 键 词：Α-突触核蛋白 MES23.5细胞 N-甲基-D-天门冬氨酸 内在化 

分 类 号：Q189[生物学—神经生物学]