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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Format: | Article |
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Nature Portfolio
2017-02-01
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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. |
first_indexed | 2024-12-22T08:43:42Z |
format | Article |
id | doaj.art-db9279e8479c4eafbe4a3235a3fa6f72 |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-12-22T08:43:42Z |
publishDate | 2017-02-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
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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