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Piezo1 haploinsufficiency does not alter mechanotransduction in mouse cochlear outer hair cells
Author(s) -
Corns Laura F.,
Marcotti Walter
Publication year - 2016
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12701
Subject(s) - mechanotransduction , mechanosensitive channels , piezo1 , stereocilia (inner ear) , cochlea , hair cell , kinocilium , inner ear , charybdotoxin , utricle , ion channel , microbiology and biotechnology , chemistry , anatomy , receptor potential , biology , biophysics , potassium channel , receptor , biochemistry
The mechanoelectrical transducer ( MET ) channels located at the stereocilia tip of cochlear hair cells are crucial to convert the mechanical energy of sound into receptor potentials, but the identity of its pore‐forming subunits remains uncertain. Piezo1 , which has been identified in the transcriptome of mammalian cochlear hair cells, encodes a transmembrane protein that forms mechanosensitive channels in other tissues. We investigated the properties of the MET channel in outer hair cells ( OHC s) of Piezo1 mice (postnatal day 6–9). The MET current was elicited by deflecting the hair bundle of OHC s using sinewave and step stimuli from a piezo‐driven fluid jet. Apical and basal OHC s were investigated because the properties of the MET channel vary along the cochlea. We found that the maximal MET current amplitude and the resting open probability of the MET channel in OHC s were similar between Piezo1 +/− haploinsufficient mice and wild‐type littermates. The sensitivity to block by the permeant MET channel blocker dihydrostreptomycin was also similar between the two genotypes. Finally, the anomalous mechano‐gated current, which is activated by sheer force and which is tip‐link independent, was unaffected in OHC s from Piezo1 +/− haploinsufficient mice. Our results suggest that Piezo1 is unlikely to be a component of the MET channel complex in mammalian cochlear OHC s.

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