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.
出处
《首都医科大学学报》
CAS
北大核心
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)~~
