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; Ian J. Russell

doi:10.1063/1.5038499

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, Ian J. Russell

Research output: Chapter in Book/Conference proceeding with ISSN or ISBN › Conference 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-1Cx30^A88V/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-1Cx30^A88V/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-1Cx30^A88V/A88V mice. Yet, the saturating amplitudes of cochlear microphonic potentials in CD-1Cx30^A88V/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 language	English
Title of host publication	To the Ear and Back Again - Advances in Auditory Biophysics
Subtitle of host publication	Proceedings of the 13th Mechanics of Hearing Workshop
Publisher	American Institute of Physics Inc.
Volume	1965
ISBN (Electronic)	9780735416703
DOIs	https://doi.org/10.1063/1.5038499
Publication status	Published - 31 May 2018
Event	13th Mechanics of Hearing Workshop: To the Ear and Back Again - Advances in Auditory Biophysics, MoH 2017 - St. Catharines, Canada Duration: 19 Jun 2017 → 24 Jun 2017

Publication series

Name	AIP Conference Proceedings
Number	1
Volume	1965
ISSN (Print)	0094-243X
ISSN (Electronic)	1551-7616

Workshop

Workshop	13th Mechanics of Hearing Workshop: To the Ear and Back Again - Advances in Auditory Biophysics, MoH 2017
Country	Canada
City	St. Catharines
Period	19/06/17 → 24/06/17

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

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Andrei Lukashkin
- A.Lukashkin@brighton.ac.uk
Person: Academic
Ian Russell
- I.Russell@brighton.ac.uk
- School of Pharmacy and Biomolecular Sci - Professor of Neurobiology
- Centre for Stress and Age-Related Disease
- Sensory Neuroscience Research and Enterprise Group
Person: Academic

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

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.",

author = "Lukashkina, {Victoria A.} and Snezana Levic and Nicola Strenzke and Lukashkin, {Andrei N.} and Russell, {Ian J.}",

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; 13th Mechanics of Hearing Workshop: To the Ear and Back Again - Advances in Auditory Biophysics, MoH 2017 ; Conference date: 19-06-2017 Through 24-06-2017",

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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 ISBN › Conference contribution with ISSN or ISBN

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AU - Russell, Ian J.

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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

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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

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

Abstract

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Bibliographical note

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Andrei Lukashkin

Ian Russell

Cite this