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.
Ultrasonic hearing is exploited for hunting and navigation as in echolocation by microbats and bottleneck dolphins and for social communication like ultrasonic vocalization by mice and rats. However, the molecular basis for ultrasonic hearing is not known yet. Here we show that knockout of the mechanosensitive ion channel Piezo2 in cochlear outer hair cells disrupts the USH but not the low-frequency hearing in mice, as shown by audiometry, acoustically-associative learning behavior, and pup-retrieval behavior. Together, our study demonstrates that Piezo2 is molecularly essential for ultrasonic vocalization based communication in mouse social lives.
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