Active cochlear amplification is dependent on supporting cell gap junctions

Abstract

Mammalian hearing relies upon active cochlear mechanics, which arises from outer hair cell (OHC) electromotility and hair bundle movement, to amplify acoustic stimulations increasing hearing sensitivity and frequency selectivity. Here we describe the novel finding that gap junctions between cochlear supporting cells also have a critical role in active cochlear amplification in vivo. We find that targeted-deletion of connexin26 (Cx26) in Deiters cells (DCs) and outer pillar cells (OPCs), which constrain OHCs standing on the basilar membrane, causes a leftward shift in OHC electromotility towards hyperpolarization, and reduces active cochlear amplification with hearing loss. Coincident with large reduction in distortion product otoacoustic emission (DPOAE) and severe hearing loss at high frequencies, the shift is larger in shorter OHCs. Our study demonstrates that active cochlear amplification in vivo is dependent on supporting cell gap junctions. These new findings also show that Cx26 deficiency can reduce active cochlear amplification to induce hearing loss.