PIEZO2 mediates ultrasonic hearing via cochlear outer hair cells in mice.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 34244441.
- Also identified by DOI 10.1073/pnas.2101207118 and PMC identifier 8285978.
- Licence recorded as CC BY-NC-ND.
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Abstract
Ultrasonic hearing and vocalization are the physiological mechanisms controlling echolocation used in hunting and navigation by microbats and bottleneck dolphins and for social communication by mice and rats. The molecular and cellular basis for ultrasonic hearing is as yet unknown. Here, we show that knockout of the mechanosensitive ion channel PIEZO2 in cochlea disrupts ultrasonic- but not low-frequency hearing in mice, as shown by audiometry and acoustically associative freezing behavior. Deletion of <i>Piezo2</i> in outer hair cells (OHCs) specifically abolishes associative learning in mice during hearing exposure at ultrasonic frequencies. Ex vivo cochlear Ca<sup>2+</sup> imaging has revealed that ultrasonic transduction requires both PIEZO2 and the hair-cell mechanotransduction channel. The present study demonstrates that OHCs serve as effector cells, combining with PIEZO2 as an essential molecule for ultrasonic hearing in mice.
Medical subject headings
- Hair Cells, Auditory, Outer
- Hearing
- Ion Channels
- Ultrasonics