School of Life Sciences, Tsinghua University, Beijing, China 100084.
IDG (International Data Group)/McGovern Institute for Brain Research at Tsinghua University, Tsinghua University, Beijing, China 100084.
Proc Natl Acad Sci U S A. 2021 Jul 13;118(28). doi: 10.1073/pnas.2101207118.
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 in outer hair cells (OHCs) specifically abolishes associative learning in mice during hearing exposure at ultrasonic frequencies. Ex vivo cochlear Ca 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.
超声听觉和发声是控制回声定位的生理机制，微蝠和瓶鼻海豚利用回声定位进行捕猎和导航，老鼠利用回声定位进行社交沟通。超声听觉的分子和细胞基础目前尚不清楚。在这里，我们发现耳蜗中的机械敏感离子通道 PIEZO2 敲除会破坏小鼠的超声听觉，但不会破坏低频听觉，这可以通过听力测试和声音联想性冻结行为来证明。在外毛细胞（OHCs）中特异性删除 会特异性地消除小鼠在听到超声频率时的听觉暴露过程中的联想学习。离体耳蜗钙成像显示，超声转导需要 PIEZO2 和毛细胞机械转导通道。本研究表明，OHCs 作为效应细胞，与 PIEZO2 一起作为小鼠超声听觉的必需分子。
