Repeated induction of a temporary threshold shift (TTS) may result in a permanent threshold shift (PTS) and is thought to be associated with early onset of age-related hearing loss (ARHL). The possibility that a PTS might be induced by administration of repeated TTS-inducing noise exposures (NEs) over a short period during early adulthood has not been formally investigated. We aimed to investigate possible cumulative acoustic overstimulation effects that permanently shift the auditory threshold. Young adult C57BL/6J mice were exposed twice to moderate white noise in an experimental design that minimized the effects of aging. The first exposure resulted in a reversible noise-induced hearing loss (NIHL) measured as recoverable alterations in auditory brainstem response (ABR) thresholds, waveform amplitudes, and numbers of ribbon synapses. The second NE with the same parameters caused persistent threshold shifts, wave I amplitude reductions, wave IV/I ratio enhancements, and synaptic losses, even though recovery time sufficient for a TTS had been provided. The pattern of PTS resembled NIHL since the observed impairments tonotopically followed the power spectrum of the noise insult, rather than ARHL, which distributes at higher frequencies. No significant changes were observed in the control group as the mice aged. To conclude, our results demonstrate a cumulative effect of repetitive TTS-inducing NE on hearing function and synaptic plasticity that does not cause premature ARHL, thereby providing insight into the pathophysiological mechanisms underlying NIHL and ARHL.

中文翻译：

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重复的适度声音暴露会导致小鼠耳蜗带状突触积累创伤。

反复诱发暂时性阈值漂移（TTS）可能导致永久性阈值漂移（PTS），并被认为与年龄相关性听力损失（ARHL）的早期发作有关。成年早期在短时间内反复服用引起TTS诱导的噪声暴露（NEs）可能诱发PTS的可能性尚未得到正式研究。我们旨在研究可能永久改变听觉阈值的累积声过度刺激效应。在使衰老影响最小化的实验设计中，成年C57BL / 6J幼鼠两次暴露于中等白噪声。第一次暴露导致可逆的噪音诱发的听力损失（NIHL），以听觉脑干反应（ABR）阈值，波形幅度和色带突触的数量的可恢复改变来衡量。即使提供了足够的TTS恢复时间，具有相同参数的第二个NE也会导致持续的阈值偏移，I波幅度减小，IV / I波比例增加和突触损失。PTS的模式类似于NIHL，因为观察到的损伤在听觉上遵循噪声侮辱的功率谱，而不是分布在较高频率的ARHL的功率谱。随年龄增长，对照组中未观察到明显变化。总而言之，我们的研究结果表明，反复诱导TTS的NE对听力功能和突触可塑性的累积作用不会引起过早的ARHL，从而为了解NIHL和ARHL的病理生理机制提供了见识。即使已经提供了足够的TTS恢复时间，IV / I波比率增强和突触丢失。PTS的模式类似于NIHL，因为观察到的损伤在听觉上遵循噪声侮辱的功率谱，而不是分布在较高频率的ARHL的功率谱。随年龄增长，对照组中未观察到明显变化。总而言之，我们的研究结果表明，反复诱导TTS的NE对听力功能和突触可塑性的累积作用不会引起过早的ARHL，从而为了解NIHL和ARHL的病理生理机制提供了见识。即使已经提供了足够的TTS恢复时间，IV / I波比率增强和突触丢失。PTS的模式类似于NIHL，因为观察到的损伤在听觉上遵循噪声侮辱的功率谱，而不是分布在较高频率的ARHL。随年龄增长，对照组中未观察到明显变化。总而言之，我们的研究结果表明，反复诱导TTS的NE对听力功能和突触可塑性的累积作用不会引起过早的ARHL，从而为了解NIHL和ARHL的病理生理机制提供了见识。而不是以较高频率分布的ARHL。随年龄增长，对照组中未观察到明显变化。总而言之，我们的研究结果表明，反复诱导TTS的NE对听力功能和突触可塑性的累积作用不会引起过早的ARHL，从而为了解NIHL和ARHL的病理生理机制提供了见识。而不是以较高频率分布的ARHL。随年龄增长，对照组中未观察到明显变化。总而言之，我们的研究结果表明，反复诱导TTS的NE对听力功能和突触可塑性的累积作用不会引起过早的ARHL，从而为了解NIHL和ARHL的病理生理机制提供了见识。