This experiment reveals that lidocaine reverses auditory cortex changes induced by quinine, suggesting neural ties to tinnitus.
Hypothesis This study investigated whether intravenous lidocaine reverses auditory cortex changes induced by systemic quinine administration. Background Quinine, like salicylate, is known to induce tinnitus. Previous studies have shown that salicylate-induced changes in the auditory cortex can be reversed by lidocaine, a compound known to suppress tinnitus. If lidocaine also reverses quinine-induced changes, it would further support the association between these neural changes and the presence of tinnitus. Methods Healthy male albino Hartley guinea pigs received systemic quinine, followed by intravenous lidocaine. Extracellular recordings were obtained from the primary auditory cortex and dorsocaudal areas across four sessions: baseline (control), two post-quinine sessions, and a post-lidocaine session. Results A total of 156 single units in the primary auditory cortex and 159 single units in the dorsocaudal areas were recorded from 10 guinea pigs. Quinine administration significantly elevated threshold in both primary auditory cortex (first post-quinine session: mean, 3.2 dB; second post-quinine session: mean, 16.2 dB) and dorsocaudal areas (first post-quinine session: mean, 3.9 dB; second post-quinine session: mean, 11.0 dB), but lidocaine did not induce further threshold changes. However, quinine-induced alterations in Q 10dB value and spontaneous firing activity were reversed by lidocaine in both the primary auditory cortex and dorsocaudal areas. Conclusion The reversal of quinine-induced changes in Q 10dB value and spontaneous firing activity by lidocaine suggests that these neural alterations are related to tinnitus. Similar results with salicylate further support the association between cortical changes and tinnitus, pointing to a possible shared central mechanism.
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Kenmochi et al. (2025) studied this question.
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