Liu Yanxing, Li Xuepei, Ma Changsheng, Liu Junxiu, Lu Hong
Department of Neurobiology, Hebei Medical University, No. 361 Zhongshan East Road, Changan District, Shijiazhuang 050017, PR China.
Hear Res. 2005 Jul;205(1-2):271-6. doi: 10.1016/j.heares.2005.03.028.
To investigate the effects of the tinnitus inducer sodium salicylate on L-type voltage-gated calcium channels, we studied freshly dissociated inferior colliculus neurons of rats by the whole-cell voltage clamp method. Salicylate's blocking of L-type calcium channels was concentration dependent, and the IC(50) value of salicylate was estimated to be 1.99 mM. An amount of 1 mM salicylate significantly shifted the steady-state inactivation curve of L-type calcium channels about 9 mV in the hyperpolarizing direction and significantly delayed calcium channel recovery. Our results suggest that salicylate's blocking of L-type calcium channels may contribute to salicylate-induced tinnitus by decreasing GABA release in the inferior colliculus.
为研究耳鸣诱导剂水杨酸钠对L型电压门控钙通道的影响,我们采用全细胞膜片钳方法对新鲜分离的大鼠下丘神经元进行了研究。水杨酸盐对L型钙通道的阻断作用呈浓度依赖性,水杨酸盐的半数抑制浓度(IC50)值估计为1.99 mM。1 mM的水杨酸盐可使L型钙通道的稳态失活曲线在超极化方向上显著偏移约9 mV,并显著延迟钙通道的恢复。我们的结果表明,水杨酸盐对L型钙通道的阻断可能通过减少下丘中的γ-氨基丁酸(GABA)释放而导致水杨酸盐诱导的耳鸣。