On July 13, 2021, Wei Xiong's Group published 'PIEZO2 mediates ultrasonic hearing via cochlear outer hair cells in mice' in PNAS.

Significance

Some animals have evolved an adaptive ability for vocalizing and hearing ultrasonic frequencies that are inaudible to humans (> 20 kHz). For decades, it has been postulated that animals hear ultrasonic frequencies with cochlear hair cells using an identical set of mechanotransduction molecules in the hair bundles for hearing audible frequencies. Here, we show that mice lacking mechanosensitive PIEZO2 ion channels have difficulty hearing at ultrasonic frequencies, but remain remarkably sensitive to audible frequencies. Thus, animals may use a partially different mechanism for sensing ultrasonic sound emissions.

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 Piezo2 in outer hair cells (OHCs) specifically abolishes associative learning in mice during hearing exposure at ultrasonic frequencies. Ex vivo cochlear Ca2+ 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.

Article link: https://www.pnas.org/content/118/28/e2101207118