Salicylate is a medicine for anti-
inflammation with a side effect of
tinnitus. To understand the mechanisms of
tinnitus induced by
salicylate, we studied the effects of
salicylate on voltage-gated
ion channels and action potential firing rates in freshly dissociated rat pyramidal neurons in auditory cortex (AC) using the whole-cell patch technique. We found that
salicylate reduced the voltage-gated
sodium current (I(Na)), the delayed rectifier
potassium current (I(K(DR))) and the L-type voltage-gated
calcium current (I(Ca,L)) in concentration-dependent manner. An amount of 1mM
salicylate shifted the steady-state inactivation curve of I(Na) negatively by about 5mV, shifted the steady-state activation and inactivation curve of I(K(DR)) negatively by approximately 14mV and 17mV, respectively, and shifted the steady-state activation curve of I(Ca,L) negatively by about 10mV. 1mM
salicylate significantly increased the action potential firing rates, ultimately. From the results, we speculated that through affecting the voltage-gated
ion channels in AC, an important position in auditory system,
salicylate increased the firing rate of neurons and enhanced neuronal excitability on the one hand, increased the excitatory transmitters release and reduced the inhibitory transmitter release on the other hand, thus finally induced
tinnitus.