Current Response in Ca V 1.3 -/- Mouse Vestibular and Cochlear Hair Cells

Signal transmission by sensory auditory and vestibular hair cells relies upon Ca -dependent exocytosis of glutamate. The Ca current in mammalian inner ear hair cells is predominantly carried through Ca 1.3 voltage-gated Ca channels. Despite this, Ca 1.3 deficient mice ( ) are deaf but do not show an...

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Published inFrontiers in neuroscience Vol. 15; p. 749483
Main Authors Manca, Marco, Yen, Piece, Spaiardi, Paolo, Russo, Giancarlo, Giunta, Roberta, Johnson, Stuart L, Marcotti, Walter, Masetto, Sergio
Format Journal Article
LanguageEnglish
Published Switzerland 2021
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Summary:Signal transmission by sensory auditory and vestibular hair cells relies upon Ca -dependent exocytosis of glutamate. The Ca current in mammalian inner ear hair cells is predominantly carried through Ca 1.3 voltage-gated Ca channels. Despite this, Ca 1.3 deficient mice ( ) are deaf but do not show any obvious vestibular phenotype. Here, we compared the Ca current ( ) in auditory and vestibular hair cells from wild-type and mice, to assess whether differences in the size of the residual could explain, at least in part, the two phenotypes. Using 5 mM extracellular Ca and near-body temperature conditions, we investigated the cochlear primary sensory receptors inner hair cells (IHCs) and both type I and type II hair cells of the semicircular canals. We found that the residual in both auditory and vestibular hair cells from mice was less than 20% (12-19%, depending on the hair cell type and age investigated) compared to controls, indicating a comparable expression of Ca 1.3 Ca channels in both sensory organs. We also showed that, different from IHCs, type I and type II hair cells from mice were able to acquire the adult-like K current profile in their basolateral membrane. Intercellular K accumulation was still present in mice during activation, suggesting that the K -based, non-exocytotic, afferent transmission is still functional in these mice. This non-vesicular mechanism might contribute to the apparent normal vestibular functions in mice.
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ISSN:1662-4548
DOI:10.3389/fnins.2021.749483