氯化铝对急性分离的大鼠海马CA1神经元钠电流、瞬时外向钾电流和延迟整流钾电流的影响。

Effects of aluminum chloride on sodium current, transient outward potassium current and delayed rectifier potassium current in acutely isolated rat hippocampal CA1 neurons.

作者信息

Zhang Bo, Nie Aifang, Bai Wei, Meng Ziqiang

机构信息

College of Arts and Science, Beijing Union University, Beijing 100038, PR China.

出版信息

Food Chem Toxicol. 2004 Sep;42(9):1453-62. doi: 10.1016/j.fct.2004.04.006.

DOI:10.1016/j.fct.2004.04.006

PMID:15234075

Abstract

The effects of aluminum chloride (AlCl3) on sodium current (INa), the transient outward potassium (IA) and delayed rectifier potassium currents (IK) in hippocampal CA1 neurons of rats were studied using the whole cell patch-clamp technique. AlCl3 decreased INa, IA, and IK in a partly reversible, dose and voltage-dependent manner. AlCl3 prolonged the time to peak of INa, and increased the inactivation time constants of INa and IA . In addition, 1000 microM AlCl3 shifted the voltage dependence of steady-state activation of INa, IA and IK toward positive potential, and the voltage dependence of steady-state inactivation of INa, IA toward negative potential. These results imply that AlCl3 could affect the activation and inactivation courses of sodium current and potassium current of rat hippocampal CA1 neurons, which may contribute to damage of the central nervous system by aluminum.

摘要

采用全细胞膜片钳技术，研究了氯化铝（AlCl3）对大鼠海马CA1神经元钠电流（INa）、瞬时外向钾电流（IA）和延迟整流钾电流（IK）的影响。AlCl3以部分可逆的、剂量和电压依赖性方式降低INa、IA和IK。AlCl3延长了INa的峰值时间，并增加了INa和IA的失活时间常数。此外，1000微摩尔/升的AlCl3使INa、IA和IK稳态激活的电压依赖性向正电位偏移，使INa、IA稳态失活的电压依赖性向负电位偏移。这些结果表明，AlCl3可能影响大鼠海马CA1神经元钠电流和钾电流的激活和失活过程，这可能是铝对中枢神经系统造成损害的原因之一。