Roles for gap-junctions in cochlear amplification and micromechanics exposed by a conexin 30 mutation

Research output: Chapter in Book/Conference proceeding with ISSN or ISBNConference contribution with ISSN or ISBN

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 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.

Original languageEnglish
Title of host publicationTo the Ear and Back Again - Advances in Auditory Biophysics
Subtitle of host publicationProceedings of the 13th Mechanics of Hearing Workshop
PublisherAmerican Institute of Physics Inc.
Volume1965
ISBN (Electronic)9780735416703
DOIs
Publication statusPublished - 31 May 2018
Event13th Mechanics of Hearing Workshop: To the Ear and Back Again - Advances in Auditory Biophysics, MoH 2017 - St. Catharines, Canada
Duration: 19 Jun 201724 Jun 2017

Publication series

NameAIP Conference Proceedings
Number1
Volume1965
ISSN (Print)0094-243X
ISSN (Electronic)1551-7616

Workshop

Workshop13th Mechanics of Hearing Workshop: To the Ear and Back Again - Advances in Auditory Biophysics, MoH 2017
CountryCanada
CitySt. Catharines
Period19/06/1724/06/17

Fingerprint

micromechanics
mutations
mice
hair
hearing
cochlea
auditory defects
degeneration
genes
proposals
partitions
energy distribution
coding
tuning
membranes
proteins
cells

Bibliographical note

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

Cite this

Lukashkina, V. A., Levic, S., Strenzke, N., Lukashkin, A. N., & Russell, I. J. (2018). Roles for gap-junctions in cochlear amplification and micromechanics exposed by a conexin 30 mutation. In To the Ear and Back Again - Advances in Auditory Biophysics: Proceedings of the 13th Mechanics of Hearing Workshop (Vol. 1965). [100001] (AIP Conference Proceedings; Vol. 1965, No. 1). American Institute of Physics Inc.. https://doi.org/10.1063/1.5038499
Lukashkina, Victoria A. ; Levic, Snezana ; Strenzke, Nicola ; Lukashkin, Andrei N. ; Russell, Ian J. / Roles for gap-junctions in cochlear amplification and micromechanics exposed by a conexin 30 mutation. To the Ear and Back Again - Advances in Auditory Biophysics: Proceedings of the 13th Mechanics of Hearing Workshop. Vol. 1965 American Institute of Physics Inc., 2018. (AIP Conference Proceedings; 1).
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Lukashkina, VA, Levic, S, Strenzke, N, Lukashkin, AN & Russell, IJ 2018, Roles for gap-junctions in cochlear amplification and micromechanics exposed by a conexin 30 mutation. in To the Ear and Back Again - Advances in Auditory Biophysics: Proceedings of the 13th Mechanics of Hearing Workshop. vol. 1965, 100001, AIP Conference Proceedings, no. 1, vol. 1965, American Institute of Physics Inc., 13th Mechanics of Hearing Workshop: To the Ear and Back Again - Advances in Auditory Biophysics, MoH 2017, St. Catharines, Canada, 19/06/17. https://doi.org/10.1063/1.5038499

Roles for gap-junctions in cochlear amplification and micromechanics exposed by a conexin 30 mutation. / Lukashkina, Victoria A.; Levic, Snezana; Strenzke, Nicola; Lukashkin, Andrei N.; Russell, Ian J.

To the Ear and Back Again - Advances in Auditory Biophysics: Proceedings of the 13th Mechanics of Hearing Workshop. Vol. 1965 American Institute of Physics Inc., 2018. 100001 (AIP Conference Proceedings; Vol. 1965, No. 1).

Research output: Chapter in Book/Conference proceeding with ISSN or ISBNConference contribution with ISSN or ISBN

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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.

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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 -

Lukashkina VA, Levic S, Strenzke N, Lukashkin AN, Russell IJ. Roles for gap-junctions in cochlear amplification and micromechanics exposed by a conexin 30 mutation. In To the Ear and Back Again - Advances in Auditory Biophysics: Proceedings of the 13th Mechanics of Hearing Workshop. Vol. 1965. American Institute of Physics Inc. 2018. 100001. (AIP Conference Proceedings; 1). https://doi.org/10.1063/1.5038499