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豚鼠耳道内的自发性耳声发射:与组织病理学的相关性及外部音调的抑制作用

Spontaneous otoacoustic emissions in chinchilla ear canals: correlation with histopathology and suppression by external tones.

作者信息

Clark W W, Kim D O, Zurek P M, Bohne B A

机构信息

Central Institute for the Deaf, Saint Louis, MO 63110.

出版信息

Hear Res. 1984 Dec;16(3):299-314. doi: 10.1016/0378-5955(84)90119-9.

Abstract

Two cases of spontaneous otoacoustic emissions (SOAEs) have been found among a sample of 28 chinchilla ears after noise exposure, and no cases of SOAEs have been found among 28 unexposed ears. Further observations of the characteristics of SOAEs recorded in the ear canals of two chinchillas after noise exposure are described. These signals were tonal, robust, and could be suppressed by presenting external tones to the ear. Histopathological evaluation of the cochlea of emitting ears revealed discrete basal-turn lesions near the positions corresponding to the frequencies of the emissions. Behavioral threshold shifts measured in one animal after noise exposure and acoustic intermodulation distortion product behavior in the other both suggest a region of increased vibratory response of the cochlear partition near the location of the SOAE. Results from these emitting ears support a hypothesis that a punctate loss of the organ of Corti (OC) may facilitate the occurrence of an SOAE. We further hypothesize that the following conditions are both necessary and sufficient for an SOAE to occur: (1) functional disruption of a normally present biomechanical control mechanism in a region of the OC; (2) presence of functionally active OC (especially outer hair cells) adjacent to the region. The observations from ears possessing SOAEs provide strong, though indirect support for active and nonlinear models in interpreting cochlear biomechanical phenomena.

摘要

在28只经噪声暴露的灰鼠耳朵样本中发现了2例自发性耳声发射(SOAE),而在28只未暴露的耳朵中未发现SOAE病例。本文描述了对2只经噪声暴露的灰鼠耳道记录的SOAE特征的进一步观察。这些信号呈音调性、强度大,并且可以通过向耳朵施加外部音调来抑制。对有耳声发射的耳朵的耳蜗进行组织病理学评估发现,在与发射频率相对应的位置附近有离散的基底转病变。在一只动物经噪声暴露后测量的行为阈值变化以及在另一只动物中测量的声互调失真产物行为均表明,在SOAE位置附近的耳蜗隔振动反应增强区域。来自这些有耳声发射耳朵的结果支持了一种假设,即柯蒂氏器(OC)的点状损失可能促进SOAE的发生。我们进一步假设,以下条件对于SOAE的发生既是必要的也是充分的:(1)OC区域中正常存在的生物力学控制机制的功能破坏;(2)与该区域相邻存在功能活跃的OC(尤其是外毛细胞)。来自有SOAE耳朵的观察结果为解释耳蜗生物力学现象的主动和非线性模型提供了有力的(尽管是间接的)支持。

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