Salicylate ototoxicity and its implications for cochlear microphonic potential generation.

ABSTRACT

Salicylic acid causes a reversible sensori-neural hearing loss. Its ototoxicity is probably related to its effect on prestin, the motor protein of the outer hair cells. In order to gain further insight into the mechanism and implications of its ototoxicity, auditory nerve brainstem evoked responses, compound action potentials of the auditory nerve, distortion product otoacoustic emissions, and cochlear microphonic potentials (CM) and vestibular evoked potentials were recorded before and after systemic salicylate administration. These responses were depressed, except for the CM and the vestibular evoked potential. This result and additional considerations provide evidence that the extracellularly recorded CM does not represent the summation of intracellular outer hair cell receptor potentials. It is possible that the CM reflects an early stage of mechano-electrical transduction by the outer hair cells, before the activation of the cochlear amplifier and the later stages of transduction.