Hidden Hearing Loss: A View from the Brain

摘要 “隐性”听力损失的概念挑战了暂时性听阈偏移（TTS）反映听力恢复的观点。 正常的听力。最近的研究表明，在噪声暴露后，产生TTS，从而在临床上 “正常”的听力图，尽管如此，听觉神经纤维（ANF）突触仍然存在永久性损伤， 耳蜗内毛细胞隐性听力损失是一个潜在的主要健康问题，因为人类的颞骨和 ABR研究表明它在人类中很常见。在临床上， 正常的听力图反映了时间编码问题，可能是由于高阈值、低自发性听力损失、 速率ANF，其在TTS之后优先受影响。高阈值ANF的主要中枢靶点 位于耳蜗核（CN）的小细胞帽（SCC）中。高阈值ANF及其SCC靶点 显示大动态范围和卓越的上级阈值调谐和时间编码，这对于 噪声环境下的语音感知SCC占人体CN的很大比例， 因此，它在隐性听力损失的中枢机制中扮演着重要角色。SCC也是独一无二的， 内侧橄榄耳蜗（MOC）神经元的假定受体和投射区。这个问题的总体假设 建议是，SCC在阈上声音编码中起着重要作用，并且这种编码是高度 易受隐性听力损失的影响。这一系列研究的目的是阐明耳蜗- SCC-MOC电路在正常和噪声损伤的动物与隐藏的听力损失，使用最先进的 光遗传学、多通道单单位生理学、束追踪和复杂的免疫组织化学 方法.

Abstract The concept of “hidden” hearing loss challenges the idea that temporary threshold shifts (TTS) reflect a return to normal hearing. Recent studies indicate that after noise-exposure that produces TTS, and thus clinically 'normal' audiograms, there is nonetheless permanent damage to auditory nerve fiber (ANF) synapses with cochlear inner hair cells. Hidden hearing loss is a potential major health issue, as human temporal bone and ABR studies suggest it is common in humans. The remaining perceptual deficits in humans with clinically normal audiograms reflect temporal coding problems likely due to loss of the high threshold, low spontaneous rate ANFs, which are preferentially affected after TTS. The primary central targets of high-threshold ANFs reside in the small cell cap (SCC) of the cochlear nucleus (CN). High-threshold ANFs and their SCC targets display large dynamic ranges and superior suprathreshold tuning and temporal coding, which are essential for speech perception in noisy environments. The SCC occupies a large proportion of the CN in humans and is therefore poised to play a major role in central mechanisms of hidden hearing loss. The SCC is unique also as a putative recipient and projection area of medial olivocochlear (MOC) neurons. The overall hypothesis of this proposal is that the SCC plays a major role in suprathreshold sound coding and that this coding is highly susceptible to degradation by hidden hearing loss. The goal of this series of studies is to elucidate the cochlea- SCC-MOC circuit in normal and noise-damaged animals with hidden hearing loss, using state-of-the-art optogenetics, multichannel single unit physiology, tract tracing and sophisticated immunohistochemical methods.