Amplification mode differs along the length of the mouse cochlea as revealed by connexin 26 deletion from specific gap junctions

Victoria Lukashkina; Tetsuji Yamashita; Jian Zuo; Andrei Lukashkin; Ian Russell

doi:10.1038/s41598-017-04279-3

Amplification mode differs along the length of the mouse cochlea as revealed by connexin 26 deletion from specific gap junctions

Victoria Lukashkina, Tetsuji Yamashita, Jian Zuo, Andrei Lukashkin, Ian Russell

Research output: Contribution to journal › Article › peer-review

Abstract

The sharp frequency tuning and exquisite sensitivity of the mammalian cochlea is due to active forcesdelivered 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 partitionmechanical impedance, thereby ensuring effective transfer of OHC isometric forces.

Original language	English
Article number	5185
Pages (from-to)	1-11
Number of pages	11
Journal	Scientific Reports
Volume	7
DOIs	https://doi.org/10.1038/s41598-017-04279-3
Publication status	Published - 12 Jul 2017

Bibliographical note

© The Author(s) 2017. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Andrei Lukashkin
- A.Lukashkinbrighton.acuk
Person: Academic
Ian Russell
- I.Russellbrighton.acuk
- School of Applied Sciences - Emeritus Professor
- Centre for Lifelong Health
Person: Academic

Cite this

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title = "Amplification mode differs along the length of the mouse cochlea as revealed by connexin 26 deletion from specific gap junctions",

abstract = "The sharp frequency tuning and exquisite sensitivity of the mammalian cochlea is due to active forcesdelivered by outer hair cells (OHCs) to the cochlear partition. Force transmission is mediated and modulated by specialized cells, including Deiters{\textquoteright} 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 partitionmechanical impedance, thereby ensuring effective transfer of OHC isometric forces.",

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AU - Russell, Ian

N1 - © The Author(s) 2017. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PY - 2017/7/12

Y1 - 2017/7/12

N2 - The sharp frequency tuning and exquisite sensitivity of the mammalian cochlea is due to active forcesdelivered 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 partitionmechanical impedance, thereby ensuring effective transfer of OHC isometric forces.

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Amplification mode differs along the length of the mouse cochlea as revealed by connexin 26 deletion from specific gap junctions

Abstract

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Andrei Lukashkin

Ian Russell

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