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Abstract：
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.
摘要：
噪声诱发的突触病（NIS）和隐性听力损失（NIHHL）一直是听力研究的热门话题，因为在2009年短暂的噪声暴露后，在CBA小鼠中发现了大量的突触损失，但并未引起永久性阈值偏移（PTS）。根据突触损失的数量及其与一组自发率（LSR）的听觉神经纤维（ANF）的突触的偏差，编码噪声缺陷（CIND）被认为是NIS和NIHHL受试者的主要听力困难。这种推测是基于这样的想法,即针对背景噪声的高水平的声音编码主要依赖于LSRANF。然而,由于现实生活中实验动物和人类受试者之间的噪声暴露差异，将NIS从动物数据转换为人类仍然是合理的，缺乏形态学数据和可靠的功能方法来量化或估计噪声对传入突触的损失。此外，没有明确的,可靠的数据揭示了CIND，即使在有突触丢失但没有PTS的动物中也是如此。在人类中,正面和负面报告都有。验证CIND的困难导致了对CIND是与NIS和NIHHL相关的主要缺陷的假设的重新检验，以及这一思想对LSRANF作用的理论基础。本文综述了NIS和NIHHL的研究现状，关注从动物数据到人类临床的转化困难，量化人类NIS的技术困难，以及SR理论在信号编码中存在的问题。时间波动轮廓模型被讨论作为一个潜在的替代信号编码在高声级对背景噪声，与耳蜗增益的传出控制机制有关。
