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目的了解瞬时外向钾通道和延迟整流钾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瞬时外向钾通道和延迟整流钾通道的影响。结果水杨酸钠能够抑制瞬时外向钾通道电流(IK(A))和延迟整流钾通道电流(IK(DR))的幅度,而且此抑制作用具有浓度依赖性(0.1～10mmol/L)。水杨酸钠抑制IK(A)和IK(DR)的50%抑制浓度(IC50)值分别为2.27mmol/L和0.80mmol/L。1mmol/L水杨酸钠不改变IK(A)的稳态激活曲线和稳态失活曲线的动力学特征,却将IK(DR)的稳态激活曲线和稳态失活曲线分别向超极化方向显著移动11mV和24mV。结论水杨酸钠以浓度依赖的方式抑制IK(A)和IK(DR),但是只影响IK(DR)的稳态激活和失活动力学特征。水杨酸钠对IK(A)和IK(DR)的影响,尤其对IK(DR)的影响可能与水杨酸钠导致耳鸣的机制有关。
Objective To understand the role of transient outward potassium channels and delayed rectifier potassium 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 the transient outward potassium channel and delayed rectifier potassium channel in acutely isolated rat inferior colliculus neurons. Results Sodium salicylate inhibited the amplitude of transient outward potassium channel currents (IK (A)) and delayed rectifier potassium channel currents (IK (DR)) in a concentration-dependent manner (0.1-10 mmol / L). The 50% inhibitory concentrations (IC50) of sodium salicylate for inhibiting IK (A) and IK (DR) were 2.27 mmol / L and 0.80 mmol / L, respectively. 1 mmol / L sodium salicylate did not change the dynamic characteristics of IK (A) steady-state activation curve and steady-state inactivation curve, but IK (DR) steady-state activation curve and steady- The direction of the significant shift 11mV and 24mV. Conclusions Sodium salicylate inhibits IK (A) and IK (DR) in a concentration-dependent manner, but only affects the steady state activation and inactivation kinetics of IK (DR). The effects of sodium salicylate on IK (A) and IK (DR), especially IK (DR), may be related to the mechanism of salicylate-induced tinnitus.