TY - GEN
T1 - Roles for gap-junctions in cochlear amplification and micromechanics exposed by a conexin 30 mutation
AU - Lukashkina, Victoria A.
AU - Levic, Snezana
AU - Strenzke, Nicola
AU - Lukashkin, Andrei N.
AU - Russell, Ian J.
N1 - Roles for gap-junctions in cochlear amplification and micromechanics exposed by a conexin 30 mutation, Victoria A. Lukashkina, Snezana Levic, Nicola Strenzke, Andrei N. Lukashkin and Ian J. Russell, AIP Conference Proceedings 2018 1965:1
PY - 2018/5/31
Y1 - 2018/5/31
N2 - 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 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 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 (OHCs) 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 OHC transmembrane potentials, determined mainly by potentials extracellular to the OHCs, drive somatic electromotility.
AB - 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 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 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 (OHCs) 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 OHC transmembrane potentials, determined mainly by potentials extracellular to the OHCs, drive somatic electromotility.
UR - http://www.scopus.com/inward/record.url?scp=85048211584&partnerID=8YFLogxK
U2 - 10.1063/1.5038499
DO - 10.1063/1.5038499
M3 - Conference contribution with ISSN or ISBN
AN - SCOPUS:85048211584
VL - 1965
T3 - AIP Conference Proceedings
BT - To the Ear and Back Again - Advances in Auditory Biophysics
PB - American Institute of Physics Inc.
ER -