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基底膜测量与行波

Basilar membrane measurements and the travelling wave.

作者信息

Johnstone B M, Patuzzi R, Yates G K

出版信息

Hear Res. 1986;22:147-53. doi: 10.1016/0378-5955(86)90090-0.

Abstract

From the original measurements of G. von Békésy (1942) until a few years ago, the basilar membrane was considered to undergo simple passive linear vibration. Recent measurements have completely altered this notion. It is now known that the BM is highly non linear and very sharply tuned. Indeed, BM can now account for most of the properties of the eighth nerve response to sound. The non linearity can be approximated by a hyperbolic function and appears to be part of an active process in the outer hair cell. At the characteristic frequency, CAP threshold (10 dB SPL) corresponds to 0.3 nm motion and the non linearity shows half saturation at 10 nm. The sigmoid shape of the full range BM input-output curve is due to the combination of a less sensitive linear passive component with the added sensitivity of the active non linear function. A hyperbolic input-output function is also present in the cochlear microphonics, and at low frequencies the half saturation value again corresponds to 10 nm BM displacement. With induced threshold loss (e.g. noise trauma) the nonlinearity disappears from the BM, but is still present in the CM. This suggests that the pathology is in the active mechanical feedback process, rather than in the receptor system. It appears that BM mechanics at low amplitudes near the resonant frequency is controlled by a nonlinear mechano-electrical transducer followed by a vulnerable, linear, active mechanism (electro-mechanical?) feeding back in positive phase onto BM vibration.

摘要

从G.冯·贝凯西1942年的最初测量直到几年前,基底膜一直被认为是进行简单的被动线性振动。最近的测量已经彻底改变了这一观念。现在已知基底膜具有高度非线性且调谐非常尖锐。实际上,基底膜现在可以解释第八神经对声音反应的大部分特性。这种非线性可以用双曲函数来近似,并且似乎是外毛细胞中一个主动过程的一部分。在特征频率处,复合动作电位阈值(10 dB声压级)对应于0.3纳米的运动,并且非线性在10纳米处显示出半饱和。整个基底膜输入 - 输出曲线的S形是由于不太敏感的线性被动成分与主动非线性函数增加的敏感性相结合。耳蜗微音器中也存在双曲输入 - 输出函数,并且在低频时半饱和值再次对应于10纳米的基底膜位移。随着诱发阈值损失(例如噪声性创伤),非线性从基底膜消失,但仍存在于耳蜗微音器中。这表明病变在于主动机械反馈过程,而不是受体系统。似乎在共振频率附近低振幅时基底膜力学是由一个非线性机电换能器控制的,随后是一个脆弱的、线性的、主动机制(机电的?)以正相位反馈到基底膜振动上。

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