首都医科大学学报 ›› 2010, Vol. 31 ›› Issue (6): 737-741.

• 帕金森病的发病机制与生物标志物 • 上一篇    下一篇

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

程芙蓉1, 李昕1, 李尧华1, 王玉兰2, 张燕莉1, 于顺1   

  1. 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
  • 收稿日期:2010-08-09 修回日期:1900-01-01 出版日期:2010-12-24 发布日期:2010-12-24
  • 通讯作者: 于顺

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

CHENG Fu-rong1, LI Xin1, LI Yao-hua1, WAND Yu-lan2, ZHANG Yan-li1, YU Shun1   

  1. 1. Department of Neurobiology, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Diseases of Ministry of Education;2. Central Laboratory, Xuanwu Hospital, Capital Medical University
  • Received:2010-08-09 Revised:1900-01-01 Online:2010-12-24 Published:2010-12-24

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。

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

Abstract: 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.

Key words: α-synuclein, MES23.5 dopaminergic cells, NMDA, internalization

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