可溶性Aβ_(25-35)对大鼠海马脑片CA3区神经元延迟整流钾电流的影响  

Effects of soluble amyloid β protein_(25-35) on delayed rectifier potassium current in CA3 neurons of rat hippocampal slices

作　　者：方丹[1] 刘振宅[1] 杨卓[2] 

机构地区：[1]天津医科大学生物医学工程系,天津300070 [2]南开大学医学院

出　　处：《天津医科大学学报》2010年第1期40-43,共4页Journal of Tianjin Medical University

摘　　要：目的:观察可溶性β淀粉样蛋白(25-35)(Aβ25-35)对大鼠海马脑片CA3区神经元延迟整流钾电流(IK)的影响,探讨可溶性Aβ25-35的神经毒性作用机制。方法:采用膜片钳全细胞记录技术观察可溶性Aβ25-35对大鼠海马脑片CA3区神经元IK的影响。结果:可溶性Aβ25-35对大鼠海马脑片CA3区神经元IK有明显抑制作用,且呈时间和电压依赖性。可溶性Aβ25-35使IK激活曲线左移,加入可溶性Aβ25-35前后IK半数激活电压分别为(5.88±0.67)mV和(-2.81±0.76)mV(P<0.05),但其斜率因子无显著改变。结论:可溶性Aβ25-35对大鼠海马脑片CA3区神经元IK的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 soluble amyloid β protein （25-35 （Aβ25-35） on delayed rectifies potassium current （IK） in CA3 neurons of rat hippocampal slices, explore the neurotoxicity mechanism of soluble Aβ25-35 in Alzheimer＇ s disease. Methods：By using whole-cell patch-clamp recording techniques, the effects of soluble Aβ25-35 on IK in CA3 neurons of rat hippocampal slices were investigated. Results： Soluble Aβ25-35 significantly suppressed IK in CA3 neurons of rat hippocampal slices in time- dependent and voltage-dependent manners. Soluble Aβ25-35 significantly shifted the steady-state activation curve of IK to more negative potential. Before and after application of Aβ25-35, the half-activation potentials of IK were （5.88±0.67）mV and （-2.8 1 ±0.76）mV, respectively（P〈0.05）,but the slope factor was not changed significantly. Conclusion： The inhibitory effect of soluble Aβ25-35 on IK may be one of the mechanisms of neurotoxicity.

关 键 词：可溶性β淀粉样蛋白(25-35) 海马脑片 延迟整流钾电流 膜片钳技术 全细胞记录 大鼠 

分 类 号：R338.8[医药卫生—人体生理学]