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 journalArticlepeer-review


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 languageEnglish
Article number5185
Pages (from-to)1-11
Number of pages11
JournalScientific Reports
Publication statusPublished - 12 Jul 2017

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