Gap Junctions and Cochlear Homeostasis |
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Authors: | H-B Zhao T Kikuchi A Ngezahayo T W White |
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Institution: | (1) Department of Surgery-Otolaryngology, University of Kentucky Medical Center, Lexington, KY, USA;(2) Department of Otolaryngology-Head and Neck Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan;(3) Institute of Biophysics, University of Hannover, Hannover, Germany;(4) Department of Physiology and Biophysics, State University of New York, Stony Brook, NY, USA |
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Abstract: | Gap junctions play a critical role in hearing and mutations in connexin genes cause a high incidence of human deafness. Pathogenesis
mainly occurs in the cochlea, where gap junctions form extensive networks between non-sensory cells that can be divided into
two independent gap junction systems, the epithelial cell gap junction system and the connective tissue cell gap junction
system. At least four different connexins have been reported to be present in the mammalian inner ear, and gap junctions are
thought to provide a route for recycling potassium ions that pass through the sensory cells during the mechanosensory transduction
process back to the endolymph. Here we review the cochlear gap junction networks and their hypothesized role in potassium
ion recycling mechanism, pharmacological and physiological gating of cochlear connexins, animal models harboring connexin
mutations and functional studies of mutant channels that cause human deafness. These studies elucidate gap junction functions
in the cochlea and also provide insight for understanding the pathogenesis of this common hereditary deafness induced by connexin
mutations.
H.-B. Zhao, T. Kikuchi, A. Ngezahayo, T. W. White contributed equally to this article |
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Keywords: | Cochlea Supporting cell Gap junction Connexin Potassium Deafness |
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