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目的了解L-型钙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L-型钙通道的影响。结果水杨酸钠抑制L-型钙通道电流(ICa,L),且具有浓度依赖性。水杨酸钠抑制ICa,L的半抑制浓度值为1.99mmol/L。水杨酸钠不影响ICa,L的电导-电压曲线和稳态激活曲线,水杨酸钠将ICa,L的稳态失活曲线向超极化方向移动8mV,并且延长ICa,L失活后恢复的时间。结论水杨酸钠对ICa,L的抑制作用,可能通过减少下丘部位γ-氨基丁酸的释放,从而导致耳鸣。
Objective To understand the role of L-type calcium 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 L-type calcium channels in isolated rat inferior colliculus neurons. Results Sodium salicylate inhibited L-type calcium channel currents (ICa, L) in a concentration-dependent manner. Sodium salicylate inhibited ICa, L half-inhibitory concentration of 1.99mmol / L. Sodium salicylate did not affect the conductance-voltage curve and steady-state activation curve of ICa, L, and sodium salicylate shifted the steady-state inactivation curve of ICa, L to hypermolality by 8mV and prolonged ICa, L inactivation Recovery time. Conclusion The inhibitory effect of sodium salicylate on ICa, L may lead to tinnitus by reducing the release of γ-aminobutyric acid in the inferior colliculus.