Carney Laurel H
Departments of Biomedical Engineering, Neuroscience, and Electrical & Computer Engineering, Del Monte Institute for Neuroscience, University of Rochester, 601 Elmwood Ave., Box 603, Rochester, NY, 14642, USA.
J Assoc Res Otolaryngol. 2018 Aug;19(4):331-352. doi: 10.1007/s10162-018-0669-5. Epub 2018 May 9.
An important topic in contemporary auditory science is supra-threshold hearing. Difficulty hearing at conversational speech levels in background noise has long been recognized as a problem of sensorineural hearing loss, including that associated with aging (presbyacusis). Such difficulty in listeners with normal thresholds has received more attention recently, especially associated with descriptions of synaptopathy, the loss of auditory nerve (AN) fibers as a result of noise exposure or aging. Synaptopathy has been reported to cause a disproportionate loss of low- and medium-spontaneous rate (L/MSR) AN fibers. Several studies of synaptopathy have assumed that the wide dynamic ranges of L/MSR AN fiber rates are critical for coding supra-threshold sounds. First, this review will present data from the literature that argues against a direct role for average discharge rates of L/MSR AN fibers in coding sounds at moderate to high sound levels. Second, the encoding of sounds at supra-threshold levels is examined. A key assumption in many studies is that saturation of AN fiber discharge rates limits neural encoding, even though the majority of AN fibers, high-spontaneous rate (HSR) fibers, have saturated average rates at conversational sound levels. It is argued here that the cross-frequency profile of low-frequency neural fluctuation amplitudes, not average rates, encodes complex sounds. As described below, this fluctuation-profile coding mechanism benefits from both saturation of inner hair cell (IHC) transduction and average rate saturation associated with the IHC-AN synapse. Third, the role of the auditory efferent system, which receives inputs from L/MSR fibers, is revisited in the context of fluctuation-profile coding. The auditory efferent system is hypothesized to maintain and enhance neural fluctuation profiles. Lastly, central mechanisms sensitive to neural fluctuations are reviewed. Low-frequency fluctuations in AN responses are accentuated by cochlear nucleus neurons which, either directly or via other brainstem nuclei, relay fluctuation profiles to the inferior colliculus (IC). IC neurons are sensitive to the frequency and amplitude of low-frequency fluctuations and convert fluctuation profiles from the periphery into a phase-locked rate profile that is robust across a wide range of sound levels and in background noise. The descending projection from the midbrain (IC) to the efferent system completes a functional loop that, combined with inputs from the L/MSR pathway, is hypothesized to maintain "sharp" supra-threshold hearing, reminiscent of visual mechanisms that regulate optical accommodation. Examples from speech coding and detection in noise are reviewed. Implications for the effects of synaptopathy on control mechanisms hypothesized to influence supra-threshold hearing are discussed. This framework for understanding neural coding and control mechanisms for supra-threshold hearing suggests strategies for the design of novel hearing aid signal-processing and electrical stimulation patterns for cochlear implants.
当代听觉科学中的一个重要主题是超阈值听力。在背景噪声中,对话语音水平下听力困难长期以来一直被认为是感音神经性听力损失的问题,包括与衰老相关的问题(老年性耳聋)。最近,正常阈值的听众出现的这种听力困难受到了更多关注,特别是与突触病变的描述相关,即由于噪声暴露或衰老导致的听觉神经(AN)纤维丧失。据报道,突触病变会导致低自发率和中自发率(L/MSR)AN纤维不成比例地丧失。几项关于突触病变的研究假设,L/MSR AN纤维率的宽动态范围对于编码超阈值声音至关重要。首先,本综述将展示文献中的数据,这些数据反对L/MSR AN纤维的平均放电率在编码中等到高强度声音时起直接作用。其次,研究超阈值水平声音的编码。许多研究中的一个关键假设是,AN纤维放电率的饱和限制了神经编码,尽管大多数AN纤维,即高自发率(HSR)纤维,在对话声音水平时平均放电率已经饱和。本文认为,低频神经波动幅度的跨频率分布,而非平均放电率,对复杂声音进行编码。如下所述,这种波动分布编码机制得益于内毛细胞(IHC)转导的饱和以及与IHC-AN突触相关的平均放电率饱和。第三,在波动分布编码的背景下,重新审视接受L/MSR纤维输入的听觉传出系统的作用。假设听觉传出系统维持并增强神经波动分布。最后,综述对神经波动敏感的中枢机制。耳蜗核神经元会增强AN反应中的低频波动,这些神经元直接或通过其他脑干核,将波动分布传递至下丘(IC)。IC神经元对低频波动的频率和幅度敏感,并将来自外周的波动分布转换为在很宽的声音水平范围内和背景噪声中都稳定的锁相放电率分布。从中脑(IC)到传出系统的下行投射完成了一个功能回路,与来自L/MSR通路的输入相结合,假设该回路维持“敏锐的”超阈值听力,这让人联想到调节眼的光学调节的视觉机制。回顾了语音编码和噪声中检测的例子。讨论了突触病变对假设影响超阈值听力的控制机制的影响。这种理解超阈值听力的神经编码和控制机制的框架为设计新型助听器信号处理和人工耳蜗电刺激模式提供了策略。