Salicylate, mefenamate, meclofenamate, and quinine on cochlear potentials

Abstract

The perilymphatic spaces of guinea pig cochleae were perfused with artificial perilymph, with and without drug, at a rate of 2.5 μl/minute for 10 minutes. The compound action potential of the auditory nerve, cochlear microphonics, and the summating potential evoked by 10 kHz tone bursts of varying intensities were recorded from a wire inserted in the basal turn scala vestibull. The endocochlear potential was recorded from the scala media. Sodium salicylate (1.25 to 10 mmol/L) reduced the magnitude of the compound action potential evoked by low-sound intensities without affecting the compound action potential evoked by high-sound intensities. Sodium salicylate also reduced cochlear microphonics and had no effect on summating potential. Cochlear perfusions of prostaglandin synthesis inhibitors, mefenamate (200 μmol/L), and meclofenamate (200 μmol/L), had no effect on the cochlear potentials. Quinine (10 to 100 μmol/L) reduced the compound action potential input-output function in a parallel fashion rather than selectively affecting the low-intensity compound action potential. Quinine (100 μmol/L) reduced cochlear microphonics and summating potential. Neither quinine (100 μmol/L) nor salicylate (5 mmol/L) affected endocochlear potential. These results suggest that salicylate-induced hearing loss is not caused by either antagonism of the hair cell transmitter or cyclooxygenase inhibition, nor is it caused by the same mechanism that causes quinine-induced hearing loss.