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Importance  Clinical observations have implied a central origin for tinnitus and potential therapeutic effects of ascorbic acid ( AA ); however, the detailed mechanisms remain undetermined.    Objective  To investigate changes in the  AA  levels and neural activity in the auditory cortex ( AC ) during salicylate‐induced tinnitus.    Methods  Rats were randomly divided into 3 groups: (1) saline group, which received an intraperitoneal saline injection; (2)  SS  group, which received an intraperitoneal sodium salicylate ( SS ) injection (350 mg/kg); and (3)  SS +Lido group, which received an intraperitoneal  SS  injection (350 mg/kg) and lidocaine delivered to the  AC  by microdialysis. For each group, we firstly used an in vivo microdialysis technique to investigate the concentrations of  AA  in the  AC ; and secondly, we recorded the neural activity in the  AC  using a single‐unit recording technique.    Results  The  AA  concentration in the  SS  group significantly increased after  SS  injection, whereas that of the saline group did not change. The  AA  concentration in the  SS +Lido group also showed an increasing trend but was significantly lower than that in the  SS  group. In the electrophysiological study, the spontaneous firing rate of the  SS  group was significantly higher than that of the saline group. In addition, the proportion of short interval discharges was also higher in the  SS  group than in the saline group. Both differences were reversed by lidocaine treatment.    Interpretation  Our data suggest that the elevation of  AA  levels in the  AC  may be related to increased neuronal activity, which may represent the mechanism underlying salicylate‐induced tinnitus.

Salicylate increased ascorbic acid levels and neuronal activity in the rat auditory cortex