Department of Otolaryngology-Head and Neck Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
Ear Institute, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
Neural Plast. 2021 Jun 9;2021:9919977. doi: 10.1155/2021/9919977. eCollection 2021.
It is widely accepted that even a single acute noise exposure at moderate intensity that induces temporary threshold shift (TTS) can result in permanent loss of ribbon synapses between inner hair cells and afferents. However, effects of repeated or chronic noise exposures on the cochlear synapses especially medial olivocochlear (MOC) efferent synapses remain elusive. Based on a weeklong repeated exposure model of bandwidth noise over 2-20 kHz for 2 hours at seven intensities (88 to 106 dB SPL with 3 dB increment per gradient) on C57BL/6J mice, we attempted to explore the dose-response mechanism of prolonged noise-induced audiological dysfunction and cochlear synaptic degeneration. In our results, mice repeatedly exposed to relatively low-intensity noise (88, 91, and 94 dB SPL) showed few changes on auditory brainstem response (ABR), ribbon synapses, or MOC efferent synapses. Notably, repeated moderate-intensity noise exposures (97 and 100 dB SPL) not only caused hearing threshold shifts and the inner hair cell ribbon synaptopathy but also impaired MOC efferent synapses, which might contribute to complex patterns of damages on cochlear function and morphology. However, repeated high-intensity (103 and 106 dB SPL) noise exposures induced PTSs mainly accompanied by damages on cochlear amplifier function of outer hair cells and the inner hair cell ribbon synaptopathy, rather than the MOC efferent synaptic degeneration. Moreover, we observed a frequency-dependent vulnerability of the repeated acoustic trauma-induced cochlear synaptic degeneration. This study provides a sight into the hypothesis that noise-induced cochlear synaptic degeneration involves both afferent (ribbon synapses) and efferent (MOC terminals) pathology. The pattern of dose-dependent pathological changes induced by repeated noise exposure at various intensities provides a possible explanation for the complicated cochlear synaptic degeneration in humans. The underlying mechanisms remain to be studied in the future.
人们普遍认为，即使是单次中等强度的急性噪声暴露，导致暂时性阈移（TTS），也会导致内毛细胞和传入纤维之间的带状突触永久性丧失。然而，重复或慢性噪声暴露对耳蜗突触，特别是内侧橄榄耳蜗（MOC）传出突触的影响仍然难以捉摸。基于为期一周的重复暴露模型，对 C57BL/6J 小鼠进行 2-20 kHz 的带宽噪声暴露，每周 7 次，每次 2 小时，强度为 88 至 106 dB SPL，每梯度增加 3 dB，我们试图探索长期噪声诱导的听力功能障碍和耳蜗突触退化的剂量反应机制。在我们的结果中，反复暴露于相对低强度噪声（88、91 和 94 dB SPL）的小鼠在听觉脑干反应（ABR）、带状突触或 MOC 传出突触上没有明显变化。值得注意的是，反复暴露于中度强度噪声（97 和 100 dB SPL）不仅导致听力阈值移位和内毛细胞带状突触病，还损害了 MOC 传出突触，这可能导致耳蜗功能和形态的复杂损伤模式。然而，反复暴露于高强度噪声（103 和 106 dB SPL）主要引起 PTS，同时伴有外毛细胞耳蜗放大器功能和内毛细胞带状突触病的损伤，而不是 MOC 传出突触的退化。此外，我们观察到重复声创伤诱导的耳蜗突触退化对频率的依赖性易损性。这项研究为噪声诱导的耳蜗突触退化涉及传入（带状突触）和传出（MOC 末梢）病理学的假设提供了一个视角。不同强度重复噪声暴露引起的剂量依赖性病理变化模式为人类复杂的耳蜗突触退化提供了一个可能的解释。其潜在机制有待进一步研究。
