Mechanotransduction is required for establishing and maintaining mature inner hair cells and regulating efferent innervation

In the adult auditory organ, mechanoelectrical transducer (MET) channels are essential for transducing acoustic stimuli into electrical signals. In the absence of incoming sound, a fraction of the MET channels on top of the sensory hair cells are open, resulting in a sustained depolarizing current....

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Veröffentlicht in:Nature communications 2018-10, Vol.9 (1), p.4015-15, Article 4015
Hauptverfasser: Corns, Laura F., Johnson, Stuart L., Roberts, Terri, Ranatunga, Kishani M., Hendry, Aenea, Ceriani, Federico, Safieddine, Saaid, Steel, Karen P., Forge, Andy, Petit, Christine, Furness, David N., Kros, Corné J., Marcotti, Walter
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Sprache:eng
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Zusammenfassung:In the adult auditory organ, mechanoelectrical transducer (MET) channels are essential for transducing acoustic stimuli into electrical signals. In the absence of incoming sound, a fraction of the MET channels on top of the sensory hair cells are open, resulting in a sustained depolarizing current. By genetically manipulating the in vivo expression of molecular components of the MET apparatus, we show that during pre-hearing stages the MET current is essential for establishing the electrophysiological properties of mature inner hair cells (IHCs). If the MET current is abolished in adult IHCs, they revert into cells showing electrical and morphological features characteristic of pre-hearing IHCs, including the re-establishment of cholinergic efferent innervation. The MET current is thus critical for the maintenance of the functional properties of adult IHCs, implying a degree of plasticity in the mature auditory system in response to the absence of normal transduction of acoustic signals. Mechanoelectrical transducer (MET) channels on the tips of inner hair cells are essential for transducing auditory sensory information. Here, the authors show that disrupting MET channel function also prevents the preservation of normal inner hair cell identity in adult mice.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-018-06307-w