A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics

Victoria A. Lukashkina, Snezana Levic, Andrei N. Lukashkin, Nicola Strenzke () and Ian J. Russell ()
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Victoria A. Lukashkina: Sensory Neuroscience Research Group, School of Pharmacy and Biomolecular Sciences, University of Brighton
Snezana Levic: Sensory Neuroscience Research Group, School of Pharmacy and Biomolecular Sciences, University of Brighton
Andrei N. Lukashkin: Sensory Neuroscience Research Group, School of Pharmacy and Biomolecular Sciences, University of Brighton
Nicola Strenzke: University Medicine Göttingen
Ian J. Russell: Sensory Neuroscience Research Group, School of Pharmacy and Biomolecular Sciences, University of Brighton

Nature Communications, 2017, vol. 8, issue 1, 1-10

Abstract: Abstract Accelerated age-related hearing loss disrupts high-frequency hearing in inbred CD-1 mice. The p.Ala88Val (A88V) mutation in the gene coding for the gap-junction protein connexin30 (Cx30) protects the cochlear basal turn of adult CD-1Cx30A88V/A88V mice from degeneration and rescues hearing. Here we report that the passive compliance of the cochlear partition and active frequency tuning of the basilar membrane are enhanced in the cochleae of CD-1Cx30A88V/A88V compared to CBA/J mice with sensitive high-frequency hearing, suggesting that gap junctions contribute to passive cochlear mechanics and energy distribution in the active cochlea. Surprisingly, the endocochlear potential that drives mechanoelectrical transduction currents in outer hair cells and hence cochlear amplification is greatly reduced in CD-1Cx30A88V/A88V mice. Yet, the saturating amplitudes of cochlear microphonic potentials in CD-1Cx30A88V/A88V and CBA/J mice are comparable. Although not conclusive, these results are compatible with the proposal that transmembrane potentials, determined mainly by extracellular potentials, drive somatic electromotility of outer hair cells.

Date: 2017
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DOI: 10.1038/ncomms14530

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