Objective:To investigate the role of spiral ganglion neuron(SGN)'s voltage-gated sodium channels in the progress of hear loss induced by sodium salicylate,to discover the mechanism of sodium salicylate on the ionic channel level.Method:The whole-cell patch clamp recording technique was used to record INa,IV curse and others electrophysiological characteristics of the acutely dissociated spiral ganglion neuron isolated from rat,and detect the effects on these electrophysiological and pharmacological characteristics.Result:(1)The sodium current(INa)was inhibited by sodium salicylate in concentration-dependent manner(10μM-1000μM).The inhibition was reversible. (2)Whether applied sodium salicyalate,INawould be activated on-60 mV and peaked on-10 mV.The voltage-gated property of INawould not be affected by sodium salicylate.(3)The steady-state activation curse of INahad no significant changed when was applying sodium salicylate 500μM.Their V1/2were -35.74±1.58 and -38.03±2.69 mV and Sloap were 10.3±1.05 and 9.65±1.935 (n=5,P<0.05).Conclusion:Our results suggest that sodium salicylate causes a reversible concentration-dependent blockade of INaand lead to a decreased action potential in SGN,which could be related to the mechanism of salicylate-induce hear loss.
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