中文摘要：

目的：了解电压门控性钠通道在水杨酸钠导致耳鸣的机制中所起的作用。方法：利用全细胞膜片钳技术研究水杨酸钠对急性分离的大鼠下丘神经元钠通道的影响。结果：水杨酸钠抑制钠通道电流（INa）,而且此抑制作用具有浓度依赖性（0.1～10.0mmol/L）。水杨酸钠抑制INa的50%抑制浓度（IC50）值为1.43mmol/L。水杨酸钠不影响INa的电导-电压曲线和稳态激活曲线,将INa的稳态失活曲线向超极化方向移动9mV。此外,水杨酸钠还延长INa的失活后恢复的时间。结论：水杨酸钠以浓度依赖的方式抑制INa,并且影响INa的稳态失活和失活后恢复的动力学特征,这可能与水杨酸钠导致耳鸣的机制有关。

英文摘要：

Objective：To investigate the mechanism of the tinnitus inducer, sodium salicylate, on voltage-gated sodium channels. Method：The effects of salicylate on voltage-gated sodium channels in freshly dissociated inferior colliculus neurons of rats were studied, using the whole-cell voltage clamp method. Result：Salicylate blocked sodium current （INa） in concentration-dependent manner （0.1-10mmol/L）. The IC50 value for the blocking action of salicylate was 1.43 mmol/L Salicylate did not affect the conductance-voltage curve and the steady-state activation curve of INa. The steady-state INa inactivation curve of INa was shifted by about 9 mV in the hyperpolarizing direction. In addition, salicylate delayed the sodium channel recovery from INa inactivation by increasing the slow time constant. Conclusion：Our results suggest that salicylate causes a concentration-dependent blockade of INa and shifts the INa inactivation curve to more hyperpolarized potentials, which could be related to the mechanism of salicylate-induced tinnitus.