TRPA1 deficiency affects cochlear potentials days after noise exposure.

TRPA1 channels are master sensors of tissue damage. We recently showed that, after acoustic trauma, TRPA1 activation in cochlear supporting cells regulates hearing sensitivity and is a component of the temporary threshold shift. In the neonate organ of Corti, TRPA1 activation in the Hensen's cells leads to prolonged calcium responses that propagate across the organ of Corti and cause long-lasting tissue displacements. In the adult cochlea, such tissue shape changes would be expected to affect the geometry and/or stiffness of the cochlear partition and, consequently, cochlear amplification. However, we still lack direct evidence of TRPA1-mediated changes to cochlear mechanics in adult mice. Here, we extracted remote cochlear microphonic (rCM) and summating potential (SP) data from auditory brainstem responses (ABRs) to evaluate noise-induced changes to these cochlear potentials that depend on TRPA1 signaling. Our results show significant differences in SP amplitudes of click-evoked ABRs between Trpa1 mice and wild-type littermates. However, five days after noise exposure, the SP differences were no longer observed likely due to an overall reduction in rCM amplitudes in the Trpa1 mice which was not seen in wild-type littermates. In addition, mice exhibited a direct current (DC) shift in the rCM elicited by an 8 kHz tone burst as the sound intensity increased, which was delayed in Trpa1 mice. Our results indicate that TRPA1 signaling after loud sound stimulation triggers changes in the cochlear transducer, but the specific mechanisms underlying these changes and whether they minimize noise-induced tissue damage remain to be elucidated.