Howard Hughes Medical Institute and Laboratory of Sensory Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Neuron. 2012 Dec 6;76(5):989-97. doi: 10.1016/j.neuron.2012.09.031.
Sensorineural hearing loss, which stems primarily from the failure of mechanosensory hair cells, changes the traveling waves that transmit acoustic signals along the cochlea. However, the connection between cochlear mechanics and the amplificatory function of hair cells remains unclear. Using an optical technique that permits the targeted inactivation of prestin, a protein of outer hair cells that generates forces on the basilar membrane, we demonstrate that these forces interact locally with cochlear traveling waves to achieve enormous mechanical amplification. By perturbing amplification in narrow segments of the basilar membrane, we further show that a cochlear traveling wave accumulates gain as it approaches its peak. Analysis of these results indicates that cochlear amplification produces negative damping that counters the viscous drag impeding traveling waves; targeted photoinactivation locally interrupts this compensation. These results reveal the locus of amplification in cochlear traveling waves and connect the characteristics of normal hearing to molecular forces.
感音神经性听力损失主要源于机械敏感毛细胞的衰竭，它改变了沿耳蜗传播声信号的行波。然而，耳蜗力学与毛细胞放大功能之间的联系仍不清楚。本研究采用一种光学技术，该技术可以靶向失活外毛细胞中的 prestin 蛋白，该蛋白在外毛细胞的基底膜上产生力，我们证明这些力与耳蜗行波局部相互作用，从而实现巨大的机械放大。通过在基底膜的狭窄段扰乱放大，我们进一步表明，当耳蜗行波接近其峰值时，它会累积增益。对这些结果的分析表明，耳蜗放大产生负阻尼，抵消了阻碍行波的粘性阻力；靶向光失活会局部中断这种补偿。这些结果揭示了耳蜗行波中放大的位置，并将正常听力的特征与分子力联系起来。
