利用全细胞膜片钳技术,在急性分离的新生大鼠海马CA3区锥体细胞上研究高效氯氰菊酯的两种组分高顺氯氰菊酯和高反氯氰菊酯对瞬时外向钾电流(transient outward potassiumcurrent,IA)和延迟整流钾电流(delayed rectifier potassiumcurrent,Ik)的影响。高顺氯氰菊酯使IA增大,而高反氯氰菊酯则使IA减小。高顺和高反氯氰菊酯均使IA激活曲线左移,反式结构还可促进IA的失活。高顺和高反氯氰菊酯均使IK减小,并使其激活曲线左移,而对IK的失活过程无影响,高反氯氰菊酯可使IK失活后恢复过程延长。结果表明,瞬时外向钾通道和延迟整流钾通道同样是高效氯氰菊酯的作用靶点,这可能是高效氯氰菊酯对哺乳动物产生毒性作用的原因之一。
The effects of β-cypermethrin (consisting of α-cypermethrin and θ-cypermethrin) on the transient outward potassium current (IA) and delayed rectifier potassium current (IK) in freshly dissociated hippocampal CA3 neurons of rats were studied using whole-cell patch-clamp technique. The results indicated that α-cypermethrin increased the value of IA and θ-cypermethrin decreased the value of IA, though both of them shifted steady activation curve of IA towards negative potential. θ-cypermethrin contributed to the inactivation of IA. The results also showed that α-cypermethrin and θ-cypermethrin decreased the value of IK, and shifted the steady state activation curve of IK towards negative potential. Both α-cypermethrin and θ-cypermethrin had no obvious effects on the inactivation of IK. θ-cypermethrin prolonged recovery process of IK. These results imply that both transient outward potassium channels and delayed rectified potassium channels are the targets of β-cypermethrin, which may explain the mechanism of toxical effects of β-cypermethrin on mammalian neurons.