Department of Neuroscience, Erasmus MC, Rotterdam, the Netherlands.
Department of Neuroscience, Erasmus MC, Rotterdam, the Netherlands.
Hear Res. 2022 Sep 15;423:108367. doi: 10.1016/j.heares.2021.108367. Epub 2021 Oct 2.
In the cochlea, mechano-electrical transduction is preceded by dynamic range compression. Outer hair cells (OHCs) and their voltage dependent length changes, known as electromotility, play a central role in this compression process, but the exact mechanisms are poorly understood. Here we review old and new experimental findings and show that (1) just audible high-frequency tones evoke an ∼1-microvolt AC receptor potential in basal OHCs; (2) any mechanical amplification of soft high-frequency tones by OHC motility would have an adverse effect on their audibility; (3) having a higher basolateral K+ conductance, while increasing the OHC corner frequency, does not boost the magnitude of the high-frequency AC receptor potential; (4) OHC receptor currents display a substantial rectified (DC) component; (5) mechanical DC responses (baseline shifts) to acoustic stimuli, while insignificant on the basilar membrane, can be comparable in magnitude to AC responses when recorded in the organ of Corti, both in the apex and the base. In the basal turn, the DC component may even exceed the AC component, lending support to Dallos' suggestion that both apical and basal OHCs display a significant degree of rectification. We further show that (6) low-intensity cochlear traveling waves, by virtue of their abrupt transition from fast to slow propagation, are well suited to transport high-frequency energy with minimal losses (∼2-dB loss for 16-kHz tones in the gerbil); (7) a 90-dB, 16-kHz tone, if transmitted without loss to its tonotopic place, would evoke a destructive displacement amplitude of 564 nm. We interpret these findings in a framework in which local dissipation is regulated by OHC motility. This article is part of the Special Issue Outer hair cell Edited by Joseph Santos-Sacchi and Kumar Navaratnam.
在内耳耳蜗中，力电转换之前存在动态范围压缩。外毛细胞（OHC）及其电压依赖性长度变化，即电运动，在外毛细胞的这种压缩过程中起着核心作用，但确切的机制尚不清楚。本文回顾了旧的和新的实验结果，并表明：（1）仅可听见的高频音会在基底 OHC 中引发约 1 微伏的交流感受器电位；（2）OHC 运动对软高频音的任何机械放大都会对其可听度产生不利影响；（3）具有更高的基底外侧 K+电导，虽然会增加 OHC 的拐角频率，但不会增强高频 AC 感受器电位的幅度；（4）OHC 感受器电流显示出相当大的整流（DC）分量；（5）对声刺激的机械 DC 响应（基线偏移），虽然在基底膜上微不足道，但在记录耳蜗器官时，其幅度可与 AC 响应相当，无论是在耳蜗的顶点还是基部；在基底回，DC 分量甚至可能超过 AC 分量，这支持了 Dallos 的观点，即顶端和基底 OHC 都表现出相当程度的整流。我们进一步表明：（6）低强度的耳蜗传播波，由于其从快速传播到缓慢传播的急剧转变，非常适合以最小的损失传输高频能量（在沙鼠中，16 kHz 音的损失约为 2 dB）；（7）如果 90 dB、16 kHz 的音无损失地传输到其音位位置，将会引起 564 nm 的破坏性位移幅度。我们在一个由 OHC 运动调节局部耗散的框架内解释这些发现。本文是由 Joseph Santos-Sacchi 和 Kumar Navaratnam 编辑的外毛细胞特刊的一部分。
