摘要
目的研究载脂蛋白E(ApoE)对大鼠皮层神经元内游离钙离子水平[Ca2+]i的影响。方法用激光共聚焦显微镜(LSCM)和Fluo-3/AM荧光探针标记检测皮层神经元钙信号瞬间动态变化;用N-甲基-D-天冬氨酸(NMDA)受体阻断剂MK-801观察ApoE4对其影响。结果ApoE4可以呈时间及浓度依赖性升高神经元内静息[Ca2+]i(P<0.01或P<0.05),MK-801可以部分阻断ApoE4所致的静息[Ca2+]i升高(P<0.05或P<0.01);而ApoE3无影响。结论急性给予ApoE4能升高神经元内静息[Ca2+]i,NMDA受体的激活可能参与了ApoE4所致的胞内钙信号改变与其神经毒作用。
Objective To investigate the acute effect of apotipoprotein E （apoE）on the intracellular free Ca2＋ of rat cortical neurons. Methods The intracellutar resting calcium level in cultured primary rat cortical neurons was measured by using confocal fluorescent imaging technique. MK-801, an N-methyl-D-aspartate （NMDA） receptor noncompetitive antagonist, was employed to test potential function of apoE4 through blocking NMDN receptor. Results Acute application of apoE4, but not apoE3, significantly increased the resting [ Ca^2＋ ] i in a dose-and time-dependent manner （P 〈 0. 01 or P 〈 0. 05）, and MK-801 partly blocked the apoE4-induced elevation of resting [ Ca^2＋ ] i （ P 〈 0. 05 or P 〈 0. 01 ）. Conclusion Acute administration of ApoFA disturbs calcium homeostasis, and the activation of NMDA receptor may play a critical role in the intracellular calcium overload induced by apoFA and neurotoxicity.
出处
《基础医学与临床》
CSCD
北大核心
2010年第1期71-74,共4页
Basic and Clinical Medicine
