Sohmer Haim
Department of Medical Neurobiology (Physiology), Institute for Medical Research - Israel-Canada, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Audiol Res. 2020 Aug 6;10(1):233. doi: 10.4081/audiores.2020.233. eCollection 2020 Jul 7.
The three modes of auditory stimulation (air, bone and soft tissue conduction) at threshold intensities are thought to share a common excitation mechanism: the stimuli induce passive displacements of the basilar membrane propagating from the base to the apex (slow mechanical traveling wave), which activate the outer hair cells, producing active displacements, which sum with the passive displacements. However, theoretical analyses and modeling of cochlear mechanics provide indications that the slow mechanical basilar membrane traveling wave may not be able to excite the cochlea at threshold intensities with the frequency discrimination observed. These analyses are complemented by several independent lines of research results supporting the notion that cochlear excitation at threshold may not involve a passive traveling wave, and the fast cochlear fluid pressures may directly activate the outer hair cells: opening of the sealed inner ear in patients undergoing cochlear implantation is not accompanied by threshold elevations to low frequency stimulation which would be expected to result from opening the cochlea, reducing cochlear impedance, altering hydrodynamics. The magnitude of the passive displacements at threshold is negligible. Isolated outer hair cells in fluid display tuned mechanical motility to fluid pressures which likely act on stretch sensitive ion channels in the walls of the cells. Vibrations delivered to soft tissue body sites elicit hearing. Thus, based on theoretical and experimental evidence, the common mechanism eliciting hearing during threshold stimulation by air, bone and soft tissue conduction may involve the fast-cochlear fluid pressures which directly activate the outer hair cells.
人们认为，在阈值强度下的三种听觉刺激模式（气导、骨导和软组织传导）共享一种共同的兴奋机制：刺激会引起基底膜从底部向顶部传播的被动位移（缓慢的机械行波），从而激活外毛细胞，产生主动位移，主动位移与被动位移相加。然而，耳蜗力学的理论分析和建模表明，在阈值强度下，缓慢的机械基底膜行波可能无法以观察到的频率辨别能力来刺激耳蜗。这些分析得到了几条独立研究结果的补充，这些结果支持阈值时的耳蜗兴奋可能不涉及被动行波这一观点，并且快速的耳蜗内流体压力可能直接激活外毛细胞：接受人工耳蜗植入的患者打开封闭的内耳时，低频刺激的阈值并未升高，而打开耳蜗、降低耳蜗阻抗、改变流体动力学本应导致阈值升高。阈值时被动位移的幅度可以忽略不计。液体中的分离外毛细胞对流体压力表现出调谐的机械运动性，流体压力可能作用于细胞壁上的拉伸敏感离子通道。传递到身体软组织部位的振动会引发听觉。因此，基于理论和实验证据，在气导、骨导和软组织传导的阈值刺激过程中引发听觉的共同机制可能涉及直接激活外毛细胞的快速耳蜗内流体压力。
