| Literature DB >> 34235622 |
Ting Fan1,2, Meng-Ya Xiang1,2, Ruo-Qiao Zhou1,2, Wen Li1,2, Li-Qin Wang1, Peng-Fei Guan1,2, Geng-Lin Li3, Yun-Feng Wang4,5, Jian Li6.
Abstract
Sodium salicylate is an anti-inflammatory medication 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 intracellular 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.Entities:
Keywords: CaV1.3 channel; Calcium current; Exocytosis; Inner hair cell; Salicylate; Tinnitus; Whole-cell patch clamp
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Year: 2021 PMID: 34235622 PMCID: PMC8782992 DOI: 10.1007/s12264-021-00747-z
Source DB: PubMed Journal: Neurosci Bull ISSN: 1995-8218 Impact factor: 5.271