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钾通道活动抑制与载脂蛋白E4引发的经由NMDA受体

  钾通道活动抑制与载脂蛋白E4引发的经由NMDA受体的钙超载有关

  秦颖1,杨力凡2,翁雨藤2,骆小莉2

  (1. 上海东方医院,同济大学医学院,200092; 2. 同济大学医学院)

  摘要:在众多关注载脂蛋白E的ε4 单体与阿尔茨海默病之间联系的机制中,我们的研究关注于其与钙稳态失调之间的关系。在急性分离的海马神经元上,我们观察到1) apoE4快速320 大幅度的升高神经元的胞内游离钙离子浓度,该作用呈现剂量和时间依赖性,并不可逆转;2) 从细胞外液中移除钙离子,可消除apoE4引发的胞内钙离子升高;3) nicardipine 对apoE4的升钙作业几乎没有影响,而MK-801 在很大幅度上可以阻断apoE4的作用;并且4) 钾通道的激动剂可以抑制apoE4的升钙作用。上述实验结果表明,apoE4经由NMDA受体,而非L型钙通道引发神经元的胞内钙离子浓度升高。在此过程中,钾通道的活动的抑制与此密切相关。

  关键词:载脂蛋白E4;钙内流;钾通道

  中图分类号:R338

  Potassium Channels Depression is involved in the Apolipoprotein E4 enhanced Calcium Influx via N-Methyl-D-Aspartate receptor

  Qin Ying1, Yang Lifan2, Weng Yuteng2, Luo Xiaoli2

  (1. East Hospital, Tongji University School of Medicine, 200092; 2. Tongji University School of Medicine)

  Foundations: National Nature Science Foundation of China (81200823), Specialized Research Fund for the Doctoral Program of Higher Education (20100072120052) Brief author introduction:Qin Ying (1976-), Female, PhD,Physiology.

  Abstract: Among many suggested mechanisms of the association between the ε4 allele of apoplipoprotein E gene (APOE) and Alzheimer’s disease (AD), the present study focused on the link of apoE4 to Ca2+ homeostasis. On the acutely isolated hippocampal neurons, our observation showed that: 1) apoE4 increased the [Ca2+]i greatly and immediately. It was in a dose- and time- dependent manner, and irreversible; 2) removing Ca2+ from external solution abolished apoE4's effect on [Ca2+]i; 3) nicardipine showed little effect on apoE4-elicited [Ca2+]i increasing, while MK-801 almost blocked the apoE4-induced Ca2+ influx; and 4) pretreatment with K+ channel opener significantly reduced the apoE4-induced [Ca2+]i increasing. The results suggest that apoE4 increased [Ca2+]i by way of NMDA receptor channels but not L-type Ca2+ channels; and the depression of K+ channel activities was involved in this effects of apoE4.

  Key words: Apolipoprotein E4, calcium influx, potassium channel

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