Ripley Sara, Xia Li, Zhang Zhen, Aiken Steve J, Wang Jian
School of Communication Sciences and Disorders, Dalhousie University, Halifax, NS, Canada.
Department of Otolaryngology-Head and Neck Surgery, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Mianyang, China.
Front Neurosci. 2022 May 23;16:893542. doi: 10.3389/fnins.2022.893542. eCollection 2022.
Noise induced synaptopathy (NIS) and hidden hearing loss (NIHHL) have been hot topic in hearing research since a massive synaptic loss was identified in CBA mice after a brief noise exposure that did not cause permanent threshold shift (PTS) in 2009. Based upon the amount of synaptic loss and the bias of it to synapses with a group of auditory nerve fibers (ANFs) with low spontaneous rate (LSR), coding-in-noise deficit (CIND) has been speculated as the major difficult of hearing in subjects with NIS and NIHHL. This speculation is based upon the idea that the coding of sound at high level against background noise relies mainly on the LSR ANFs. However, the translation from animal data to humans for NIS remains to be justified due to the difference in noise exposure between laboratory animals and human subjects in real life, the lack of morphological data and reliable functional methods to quantify or estimate the loss of the afferent synapses by noise. Moreover, there is no clear, robust data revealing the CIND even in animals with the synaptic loss but no PTS. In humans, both positive and negative reports are available. The difficulty in verifying CINDs has led a re-examination of the hypothesis that CIND is the major deficit associated with NIS and NIHHL, and the theoretical basis of this idea on the role of LSR ANFs. This review summarized the current status of research in NIS and NIHHL, with focus on the translational difficulty from animal data to human clinicals, the technical difficulties in quantifying NIS in humans, and the problems with the SR theory on signal coding. Temporal fluctuation profile model was discussed as a potential alternative for signal coding at high sound level against background noise, in association with the mechanisms of efferent control on the cochlea gain.
自2009年在CBA小鼠短暂噪声暴露后发现大量突触损失（该噪声暴露未导致永久性阈移）以来，噪声性突触病变（NIS）和隐匿性听力损失（NIHHL）一直是听力研究中的热门话题。基于突触损失的数量以及其对具有低自发放电率（LSR）的一组听神经纤维（ANF）突触的偏向性，噪声编码缺陷（CIND）被推测为NIS和NIHHL患者听力方面的主要难题。这种推测基于这样一种观点，即高水平声音相对于背景噪声的编码主要依赖于LSR ANF。然而，由于实验动物与现实生活中的人类受试者在噪声暴露方面存在差异，缺乏形态学数据以及可靠的功能方法来量化或估计噪声引起的传入突触损失，从动物数据到人类的NIS转化仍有待验证。此外，即使在有突触损失但无PTS的动物中，也没有明确、有力的数据揭示CIND。在人类中，既有肯定的报告，也有否定的报告。验证CIND的困难导致人们重新审视CIND是与NIS和NIHHL相关的主要缺陷这一假设，以及该观点在LSR ANF作用方面的理论基础。本综述总结了NIS和NIHHL的研究现状，重点关注从动物数据到人类临床研究的转化困难、量化人类NIS的技术困难以及信号编码的SR理论存在的问题。结合传出神经对耳蜗增益的控制机制，讨论了时间波动轮廓模型作为高水平声音相对于背景噪声进行信号编码的潜在替代方案。
