Preyer S, Gummer A W
Department of Otolaryngology, University of Tübingen, Germany.
Audiol Neurootol. 1996 Jan-Feb;1(1):3-11. doi: 10.1159/000259185.
The sound-induced travelling wave in the mammalian cochlea is believed to be enhanced and sharpened by a positive-feedback mechanism, causing the passive, linear growth function of the basilar membrane (BM) to become nonlinear. Based on direct measurements of the receptor potential of isolated outer hair cells, it is shown here how nonlinear BM motion might be due predominantly to the nonlinear growth function of the receptor potential. Since intensity coding in the inner ear is supposed to depend on an interaction of nonlinear BM motion with afferent fibres of different synaptic thresholds, intensity coding is expected to be directly dependent on the mechanoelectrical transduction of outer hair cells (OHC). According to the present experimental data and the feedback concept of outer hair cell action, disruption of the mechanoelectrical transduction of OHC leads to both a reduction of gain and linearizing of the response; that is, to both hearing loss and loudness recruitment.
哺乳动物耳蜗中由声音诱发的行波被认为是通过正反馈机制得到增强和锐化的,这使得基底膜(BM)的被动线性生长函数变为非线性。基于对分离的外毛细胞受体电位的直接测量,本文展示了非线性基底膜运动可能主要归因于受体电位的非线性生长函数。由于内耳中的强度编码被认为取决于非线性基底膜运动与具有不同突触阈值的传入纤维之间的相互作用,所以强度编码预计直接依赖于外毛细胞(OHC)的机械电转导。根据目前的实验数据和外毛细胞作用的反馈概念,外毛细胞机械电转导的破坏会导致增益降低和反应线性化,也就是说,会导致听力损失和响度重振。