二氧化硫衍生物对大鼠海马CA3区神经元瞬间外向钾电流的影响

THE EFFECT OF SO2 DERIVATIVES ON TRANSIENT OUTWARD K^+ CURRENT IN ACUTELY DISSOCIATED RAT HIPPOCAMPAL CA3 NEURONS

为研究二氧化硫(SO2)衍生物——NaHSO3,和Na2SO3(二者分子比为1:3)对大鼠海马CA3区神经元瞬间外向钾电流(IA)的影响,利用全细胞膜片钳技术,根据动力学和药理学特性分离鉴定大鼠海马CA3区神经元IA,观察SO2衍生物对IA的效应。发现SO2代谢衍生物可浓度依赖性地增大,IA,使IA增大50％的剂量为25 μmol/L。此外还与电压呈依赖关系,但不具有频率依赖性。10 μmol/L的SO2代谢衍生物不影响IA电流的激活过程,但升高了A-通道稳态失活电压,延长了A-电流失活时间。说明SO2代谢衍生物可增大大鼠海马CA3区神经元IA电流,延长A-电流的失活时间,从而影响海马神经元的膜生理感应,这可能是SO2影响神经细胞功能的机理之一。

In order to study the effect of SO2 derivatives -NaHSO3 and Na2SO3 (1:3) on transient outward K+ current in freshly dissociated hippocampal neurons of rats, with the whole cell patch clamp technique, IA was isolated based on the kinetics and pharmacological properties, and the increase effects of SO2 derivatives on IA were investigated in rat acutely isolated CA3 neurons. SO2 derivatives reversibly increased the amplitudes of IA in a concentration-dependent and voltage-dependent, but not frequency-dependent manner. Half-increase dose on IA was 25 μmol/L. 10 μmol/L SO2 derivatives did not affect the activation process of IA, while affected the inaction process rose, the half-inactivation of IA voltages and delayed the process of IA inactiration. It was found that SO2 derivatives increase the amplitude of IA in CA3 neurons, and inhibit the inactivation of IA. After SO2 derivatives application, normal sensory physiology of hippocampal neurons was affected. This variation caused by SO2 could underlie the toxical modulation of sensory input to the central nervous system.