ArticleNature communications2013
Active cochlear amplification is dependent on supporting cell gap junctions.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 88 citations in OpenAlex.
- Upregulation of ATP-purinergic P2×2 receptors in the cochlea over-amplifies hearing sensitivity leading to hyperacusis and attenuation by antagonists.bioRxiv : the preprint server for biology · 2026Article
- Connexin 26 in Hearing Health and Disease: StructuralFoundations, Mutation Mechanisms, and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Recent Progress in Mechanism-Based Therapies forInternational journal of molecular sciences · 2026Review
- Genetic and Environmental Factors Shaping Hearing Loss: Xenobiotics, Mechanisms and Translational Perspectives.Journal of xenobiotics · 2026Review
- Promotion of a new gap junction gene Cx46 (GJA3) expression in the cochlea after Cx26 (GJB2) deficiency.Hearing research · 2025Article
- Prevention and treatment of noise-induced hearing loss and cochlear synapse degeneration by potassium channel blockers in vivo.Hearing research · 2025Article
- ATP-gated P2x7 receptors express at type II auditory nerves and required for efferent hearing control and noise protection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Promotion of Cx26 mutants located in TM4 region for membrane translocation successfully rescued hearing loss.Theranostics · 2025Article
- Innexin expression and localization in the Drosophila antenna indicate gap junction or hemichannel involvement in antennal chemosensory sensilla.Cell and tissue research · 2024Article
- Abnormal Innervation, Demyelination, and Degeneration of Spiral Ganglion Neurons as Well as Disruption of Heminodes are Involved in the Onset of Deafness in Cx26 Null Mice.Neuroscience bulletin · 2024Article
- Preservation of developmental spontaneous activity enables early auditory system maturation in deaf mice.PLoS biology · 2023Article
- Cx26 heterozygous mutations cause hyperacusis-like hearing oversensitivity and increase susceptibility to noise.Science advances · 2023Article
- Sestrin 2 Deficiency Exacerbates Noise-Induced Cochlear Injury Through Inhibiting ULK1/Parkin-Mediated Mitophagy.Antioxidants & redox signaling · 2023Article
- Connexin Mutations and Hereditary Diseases.International journal of molecular sciences · 2022Review
- Cellular mechanisms of connexin-based inherited diseases.Trends in cell biology · 2022Review
- Pathological mechanisms of connexin26-related hearing loss: Potassium recycling, ATP-calcium signaling, or energy supply?Frontiers in molecular neuroscience · 2022Review
- Supporting Cells and Their Potential Roles in Cisplatin-Induced Ototoxicity.Frontiers in neuroscience · 2022Review
- Efferent neurons control hearing sensitivity and protect hearing from noise through the regulation of gap junctions between cochlear supporting cells.Journal of neurophysiology · 2022Article
- Whole exome sequencing, in silico and functional studies confirm the association of theSaudi journal of biological sciences · 2021Article
- Dynamic Spatiotemporal Expression Changes in Connexins of the Developing Primate's Cochlea.Genes · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Mammalian hearing relies upon active cochlear mechanics, which arises from outer hair cell electromotility and hair bundle movement, to amplify acoustic stimulations increasing hearing sensitivity and frequency selectivity. Here we describe the novel finding that gap junctions between cochlear supporting cells also have a critical role in active cochlear amplification in vivo. We find that targeted-deletion of connexin 26 in Deiters cells and outer pillar cells, which constrain outer hair cells standing on the basilar membrane, causes a leftward shift in outer hair cell electromotility towards hyperpolarization, and reduces active cochlear amplification with hearing loss. Coincident with large reduction in distortion product otoacoustic emission and severe hearing loss at high frequencies, the shift is larger in shorter outer hair cells. Our study demonstrates that active cochlear amplification in vivo is dependent on supporting cell gap junctions. These new findings also show that connexin 26 deficiency can reduce active cochlear amplification to induce hearing loss.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.