ArticleScientific reports2017
Amplification mode differs along the length of the mouse cochlea as revealed by connexin 26 deletion from specific gap junctions.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Preservation of developmental spontaneous activity enables early auditory system maturation in deaf mice.PLoS biology · 2023Article
- A Gap-Junction Mutation Reveals That Outer Hair Cell Extracellular Receptor Potentials Drive High-Frequency Cochlear Amplification.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Connexin Mutations and Hereditary Diseases.International journal of molecular sciences · 2022Review
- Prestin kinetics and corresponding frequency dependence augment during early development of the outer hair cell within the mouse organ of Corti.Scientific reports · 2019Article
- Revealing the morphology and function of the cochlea and middle ear with optical coherence tomography.Quantitative imaging in medicine and surgery · 2019Review
- Structure and Function of Cochlear Gap Junctions and Implications for the Translation of Cochlear Gene Therapies.Frontiers in cellular neuroscience · 2019Article
- High-resolution transcriptional dissection of in vivo Atoh1-mediated hair cell conversion in mature cochleae identifies Isl1 as a co-reprogramming factor.PLoS genetics · 2018Article
- Pannexin 1 Modulates Axonal Growth in Mouse Peripheral Nerves.Frontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The sharp frequency tuning and exquisite sensitivity of the mammalian cochlea is due to active forces delivered by outer hair cells (OHCs) to the cochlear partition. Force transmission is mediated and modulated by specialized cells, including Deiters' cells (DCs) and pillar cells (PCs), coupled by gap-junctions composed of connexin 26 (Cx26) and Cx30. We created a mouse with conditional Cx26 knock-out (Cx26 cKO) in DCs and PCs that did not influence sensory transduction, receptor-current-driving-voltage, low-mid-frequency distortion-product-otoacoustic-emissions (DPOAEs), and passive basilar membrane (BM) responses. However, the Cx26 cKO desensitizes mid-high-frequency DPOAEs and active BM responses and sensitizes low-mid-frequency neural excitation. This functional segregation may indicate that the flexible, apical turn cochlear partition facilitates transfer of OHC displacements (isotonic forces) for cochlear amplification and neural excitation. DC and PC Cx26 expression is essential for cochlear amplification in the stiff basal turn, possibly through maintaining cochlear partition mechanical impedance, thereby ensuring effective transfer of OHC isometric forces.
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