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

A point mutation in the gap-junction protein connexin 30 stops early onset age-related hearing loss. Here, the authors show that gap junctions contribute to cochlear micromechanics and that cochlear amplification is likely controlled by extracellular potentials in vicinity of the cochlear sensory ce...

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Main Authors: Victoria A. Lukashkina, Snezana Levic, Andrei N. Lukashkin, Nicola Strenzke, Ian J. Russell
Format: Article
Language:English
Published: Nature Portfolio 2017-02-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms14530
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author Victoria A. Lukashkina
Snezana Levic
Andrei N. Lukashkin
Nicola Strenzke
Ian J. Russell
author_facet Victoria A. Lukashkina
Snezana Levic
Andrei N. Lukashkin
Nicola Strenzke
Ian J. Russell
author_sort Victoria A. Lukashkina
collection DOAJ
description A point mutation in the gap-junction protein connexin 30 stops early onset age-related hearing loss. Here, the authors show that gap junctions contribute to cochlear micromechanics and that cochlear amplification is likely controlled by extracellular potentials in vicinity of the cochlear sensory cells.
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spelling doaj.art-db9279e8479c4eafbe4a3235a3fa6f722022-12-21T18:32:11ZengNature PortfolioNature Communications2041-17232017-02-018111010.1038/ncomms14530A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanicsVictoria A. Lukashkina0Snezana Levic1Andrei N. Lukashkin2Nicola Strenzke3Ian J. Russell4Sensory Neuroscience Research Group, School of Pharmacy and Biomolecular Sciences, University of BrightonSensory Neuroscience Research Group, School of Pharmacy and Biomolecular Sciences, University of BrightonSensory Neuroscience Research Group, School of Pharmacy and Biomolecular Sciences, University of BrightonDepartment of Otorhinolaryngology, University Medicine GöttingenSensory Neuroscience Research Group, School of Pharmacy and Biomolecular Sciences, University of BrightonA point mutation in the gap-junction protein connexin 30 stops early onset age-related hearing loss. Here, the authors show that gap junctions contribute to cochlear micromechanics and that cochlear amplification is likely controlled by extracellular potentials in vicinity of the cochlear sensory cells.https://doi.org/10.1038/ncomms14530
spellingShingle Victoria A. Lukashkina
Snezana Levic
Andrei N. Lukashkin
Nicola Strenzke
Ian J. Russell
A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics
Nature Communications
title A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics
title_full A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics
title_fullStr A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics
title_full_unstemmed A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics
title_short A connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics
title_sort connexin30 mutation rescues hearing and reveals roles for gap junctions in cochlear amplification and micromechanics
url https://doi.org/10.1038/ncomms14530
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