噪声诱导的暂时性阈移后，龙猫持续性听神经缺陷及自发放电率组成的改变

文献信息

中文摘要

背景： 临床听力图正常的听者仍可能在噪声中听音困难，这一问题常在“隐性听力损失”的背景下讨论。耳蜗突触病被认为是这些缺陷的潜在机制之一，但用于检测突触病的可靠生理学检测方法仍具挑战性。本研究通过耳蜗组织学、无创生理学测量和单单位听神经记录，检查了在龙猫中产生暂时性阈移（TTS）的噪声暴露的影响。方法：组织学证实暴露后内毛细胞突触持续丢失。暴露后2周，ABR阈值恢复，DPOAE水平保持，许多听神经反应特性（包括调谐和速率-水平反应指标）在存活纤维中未显示显著的暴露后差异。然而，暴露后仍存在若干阈上和时间相关的异常。结果：阈上ABR测量显示Peak 1振幅降低和Peak 5-Peak 1潜伏期延长，而单单位记录显示暴露群体中低SR纤维比例降低。在听神经时间性和调制相关指标中也观察到选择性的暴露后差异，包括首次尖峰时间变异性降低、适应后放电率增加、包络编码强度降低和包络编码延迟延长，提示阈上时间编码的残余破坏可能与噪声中听音的感知相关。结论：这些发现表明，恢复的TTS产生微妙但持续的神经变化，这些变化未被传统的基于阈值的测量完全捕捉。结果可能有助于解释为什么耳蜗突触病的诊断仍然具有挑战性，并支持使用阈上、潜伏期敏感和基于调制的生理学检测来检测耳蜗突触病的残余神经效应。

英文摘要

Listeners with clinically normal audiograms can still experience difficulty hearing in noise, a problem often discussed in the context of "hidden hearing loss". Cochlear synaptopathy has been proposed as one potential mechanism underlying these deficits, but reliable physiological assays for detecting synaptopathy remain challenging. The present study examined the effects of noise exposure that produced temporary threshold shift (TTS) in chinchillas using cochlear histology, noninvasive physiological measures, and single-unit auditory-nerve recordings. Histology confirmed persistent loss of inner-hair-cell synapses following exposure. ABR thresholds recovered and DPOAE levels were preserved 2 weeks after exposure, and many auditory-nerve response properties, including tuning and rate-level response metrics, showed no significant post-exposure differences among surviving fibers. However, several suprathreshold and timing-related abnormalities persisted after exposure. Suprathreshold ABR measures showed reduced Peak 1 amplitudes and prolonged Peak 5-Peak 1 latencies, while single-unit recordings revealed a reduced proportion of low-SR fibers in the exposed population. Selective post-exposure differences were also observed in auditory-nerve timing and modulation-related metrics, including reduced first-spike timing variability, increased adapted firing rate, reduced envelope-coding strength, and prolonged envelope-coding delay, suggesting residual disruption of suprathreshold temporal coding that may be perceptually relevant for listening in noise. These findings suggest that recovered TTS produces subtle but persistent neural changes that are not fully captured by conventional threshold-based measures. The results may help explain why diagnosis of cochlear synaptopathy remains challenging, and support the use of suprathreshold, latency-sensitive, and modulation-based physiological assays to detect residual neural effects of cochlear synaptopathy.