脊神经损伤后钠电流的变化及其离子通道机制

目的：检测脊神经切断大鼠背根节（DRG）神经元重复放电能力和钠电流的变化,并研究介导其电流变化的钠通道亚型的表达情况。方法：脊神经切断术后2～8d慢性痛大鼠模型背根节急性分离,对中等直径DRG神经元运用全细胞膜片钳技术记录神经元放电和钠电流的变化。对背根节神经元进行RT-PCR检测,分析其钠通道亚型的表达情况。结果：电流钳下,实验组DRG神经元在电流刺激下产生重复放电,而对照组神经元多诱发单个动作电位,电压钳记录发现实验组背根节神经元快钠电流和持续性钠电流幅值均明显大于对照组,PCR结果显示,Nav1.3、Nav1.7和Nav1.8通道亚型mRNA表达显著增高。结论：钠通道介导了脊神经受损模型的DRG神经元兴奋性增高,持续性钠电流可能通过调节阈下膜电位振荡的产生调节神经元兴奋性。

Change of Sodium Current and Its Ion Channels Mechanism After Spinal Nerve Injury

Objective：To detect the changes of sodium influx in the transected spinal nerve rats and to investigate the expression of the sodium channel subunits.Methods：2~8d after spinal nerve transection in rats model of chronic pain,the DRG were acutely isolated.The neuron discharge and sodium influx of medium-diameter DRG neurons were detected by the whole cell recording patch clamp tech-nique.The DRG neurons,the expression of sodium channel subunits were detected by RT-PCR.Results：the repetitive firing of DRG neurons in experiment was induced under current stimulation,However,the single action potential was induced in control.According to the voltage-clamp recordings,the amplitude of the fast and persistent sodium current of DRG neurons in experiment wAS both obviously higher than that in control group.Meanwhile,the expression of sodium channel subunits Nav1.3,Nav1.7 and Nav1.8 mRNA was obvi-ously higher.Conclusions：The sodium channel increased the excitability of DRG neurons in the spinal nerve,and the persistent sodium current could adjust the excitability of neurons by regulating the subthreshold membrane potential oscillation.