Active cochlear amplification is dependent on supporting cell gap junctions

Yan Zhu, Chun Liang, Jin Chen, Liang Zong, Guang-Di Chen and Hong-Bo Zhao ()
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Yan Zhu: University of Kentucky Medical School
Chun Liang: University of Kentucky Medical School
Jin Chen: University of Kentucky Medical School
Liang Zong: University of Kentucky Medical School
Guang-Di Chen: Center for Hearing & Deafness, SUNY
Hong-Bo Zhao: University of Kentucky Medical School

Nature Communications, 2013, vol. 4, issue 1, 1-8

Abstract: Abstract Mammalian hearing relies upon active cochlear mechanics, which arises from outer hair cell 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 connexin 26 in Deiters cells and outer pillar cells, which constrain outer hair cells standing on the basilar membrane, causes a leftward shift in outer hair cell electromotility towards hyperpolarization, and reduces active cochlear amplification with hearing loss. Coincident with large reduction in distortion product otoacoustic emission and severe hearing loss at high frequencies, the shift is larger in shorter outer hair cells. Our study demonstrates that active cochlear amplification in vivo is dependent on supporting cell gap junctions. These new findings also show that connexin 26 deficiency can reduce active cochlear amplification to induce hearing loss.

Date: 2013
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DOI: 10.1038/ncomms2806

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