非凝聚态淀粉样蛋白对大鼠海马神经元瞬时外向钾电流的影响  

The Effects of Unaggregated Amyloid β Protein(25-35) on Transient Outward Potassium Current in Rat Hippocampal CA3 Pyramidal Neurons

作　　者：李琳[1] 刘振宅[2] 贺秉军[3] 戚豫[1] 

机构地区：[1]北京大学第一医院中心实验室,100034 [2]天津医科大学生物医学工程系,300070 [3]南开大学生命科学院,天津300071

出　　处：《医学研究杂志》2008年第11期70-73,共4页Journal of Medical Research

摘　　要：目的探讨凝聚前的β淀粉样蛋白(Aβ25～35)对新生大鼠海马CA3区锥体神经元瞬时外向钾电流(IA)的影响。方法采用全细胞膜片钳技术记录非凝聚态Aβ25～35作用前后IA峰值和动力学变化。结果非凝聚态Aβ25～35对新生大鼠海马CA3区神经元IA有明显抑制作用,其效应具有时间依赖性,浓度依赖性和电压依赖性,同时使IA的激活动力学曲线和失活动力学曲线均明显左移。结论β淀粉样蛋白在凝聚成老年斑之前就对大鼠海马CA3区神经元的瞬时外向钾电流有抑制作用,可能是其产生神经毒性作用的机制之一。Objective To investigate the effects of unaggregated amyloid β protein （Aβ25-35） on transient outward potassium channel （ IA ） in Rat Hippoeampal CA3 Pyramidal Neurons. Methods Patch - clamp technique with whole cell recording was used. Results Unaggregated Aβ25-35 inhibited IA in neonatal rat hippocampal CA3 pyramidal neurons and displayed a time - ,concentration - and voltage -dependent manner;the dynamic characteristics of IA were influenced：shifted the steady- state activation and inactivation curves to left significantly. Conclusion These results suggest that the inhibition of unaggregated Aβ25-35 on transient outward potassium channel in acutely isolated hippoeampal CA3 pyramidal neurons may be an important mechanism of its toxicity,which participates in pathological changes of AD.

关 键 词：阿尔茨海默病 可溶性β淀粉样蛋白 瞬时外向钾电流 海马神经元 

分 类 号：R749.16[医药卫生—神经病学与精神病学] R972[医药卫生—临床医学]