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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。
AIM: To understand the role of voltage-gated sodium channels in the mechanism of sodium salicylate-induced tinnitus. Methods: Whole-cell patch-clamp technique was used to study the effect of sodium salicylate on acutely isolated rat inferior collicular neuronal sodium channel. Results: Sodium salicylate inhibited sodium channel current (INa), and the inhibitory effect was concentration-dependent (0.1-10.0 mmol / L). The 50% inhibitory concentration (IC50) of sodium salicylate for INa inhibition was 1.43 mmol / L. Sodium salicylate did not affect the conductivity-voltage curve and steady-state activation curve of INa, and shifted the INa steady-state inactivation curve to hypermolality by 9mV. In addition, sodium salicylate also prolongs the recovery time after inactivation of INa. CONCLUSIONS: Sodium salicylate inhibits INa in a concentration-dependent manner and affects the kinetic characteristics of INa homeostasis and recovery after inactivation, which may be related to the mechanism of sodium salicylate-induced tinnitus.