摘要Sodium salicylate is an anti-inflammatory med-ication with a side-effect of tinnitus.Here,we used mouse cochlear cultures to explore the effects of salicylate treatment on cochlear inner hair cells (IHCs).We found that IHCs showed significant damage after exposure to a high concentration of salicylate.Whole-cell patch clamp recordings showed that 1-5 mmol/L salicylate did not affect the exocytosis of IHCs,indicating that IHCs are not involved in tinnitus generation by enhancing their neuronal input.Instead,salicylate induced a larger peak amplitude,a more negative half-activation voltage,and a steeper slope factor of Ca2+ current.Using noise analysis of Ca2+ tail currents and qRT-PCR,we further found that salicylate increased the number of Ca2+ channels along with Cav1.3 expression.All these changes could act synergistically to enhance the Ca2+ influx into IHCs.Inhibition of intracel-lular Ca2+ overload significantly attenuated IHC death after 10 mmol/L salicylate treatment.These results implicate a cellular mechanism for tinnitus generation in the peripheral auditory system.