Prior work has provided extensive documentation of threshold sensitivity and sensory hair cell losses after noise exposure. It is now clear, however, that cochlear synaptic loss precedes such losses, at least at low-moderate noise doses, silencing affected neurons. To address questions of whether, and how, cochlear synaptopathy and underlying mechanisms change as noise dose is varied, we assessed cochlear physiologic and histologic consequences of a range of exposures varied in duration from 15 min to 8 h and in level from 85 to 112 dB SPL. Exposures delivered to adult CBA/CaJ mice produced acute elevations in hair cell- and neural-based response thresholds ranging from trivial (∼5 dB) to large (∼50 dB), followed by varying degrees of recovery. Males appeared more noise vulnerable for some conditions of exposure. There was little to no inner hair cell (IHC) loss, but outer hair cell (OHC) loss could be substantial at highest frequencies for highest noise doses. Synapse loss was an early manifestation of noise injury and did not scale directly with either temporary or permanent threshold shift. With increasing noise dose, synapse loss grew to ∼50%, then declined for exposures yielding permanent hair cell injury/loss. All synaptopathic, but no non-synaptopathic exposures produced persistent neural response amplitude declines; those additionally yielding permanent OHC injury/loss also produced persistent reductions in OHC-based responses and exaggerated neural amplitude declines. Findings show that widespread cochlear synaptopathy can be present with and without noise-induced sensory cell loss and that differing patterns of cellular injury influence synaptopathic outcomes.

中文翻译：

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噪声诱导的耳蜗突触病伴或不伴感觉细胞丢失。

先前的工作已经提供了有关噪声暴露后阈值敏感性和感觉毛细胞损失的大量文献资料。然而，现在清楚的是，至少在低中度噪声剂量下，耳蜗突触损失先于这种损失，使受影响的神经元沉默。为了解决随噪声剂量变化而发生的耳蜗突触病及其潜在机制是否以及如何变化的问题，我们评估了在15分钟至8小时的持续时间和85至112 dB的水平范围内变化的一系列耳蜗的生理和组织学后果SPL。传递给成年CBA / CaJ小鼠的暴露使基于毛细胞和神经的反应阈值急剧升高，范围从微不足道（〜5 dB）到大（〜50 dB），随后恢复程度不同。在某些暴露条件下，雄性似乎更容易受到噪声干扰。几乎没有甚至没有内部毛细胞（IHC）的损失，但是对于最高的噪声剂量，在最高频率下外部毛细胞（OHC）的损失可能很大。突触损失是噪声损伤的早期表现，不能随临时或永久阈值移位直接缩放。随着噪声剂量的增加，突触损失增至〜50％，然后由于暴露而下降，产生永久性的毛细胞损伤/损失。所有的突触性暴露，但没有非突触性暴露，会引起持续的神经反应幅度下降。那些额外产生永久性OHC损伤/损失的患者，也导致基于OHC的反应持续下降，并导致神经幅度过度放大。