Department of Physiology and Pharmacology, Medical College of Southeast University, Nanjing, China.
PLoS One. 2012;7(11):e49550. doi: 10.1371/journal.pone.0049550. Epub 2012 Nov 21.
Noise-exposure at levels low enough to avoid a permanent threshold shift has been found to cause a massive, delayed degeneration of spiral ganglion neurons (SGNs) in mouse cochleae. Damage to the afferent innervation was initiated by a loss of synaptic ribbons, which is largely irreversible in mice. A similar delayed loss of SGNs has been found in guinea pig cochleae, but at a reduced level, suggesting a cross-species difference in SGN sensitivity to noise. Ribbon synapse damage occurs "silently" in that it does not affect hearing thresholds as conventionally measured, and the functional consequence of this damage is not clear. In the present study, we further explored the effect of noise on cochlear afferent innervation in guinea pigs by focusing on the dynamic changes in ribbon counts over time, and resultant changes in temporal processing. It was found that (1) contrary to reports in mice, the initial loss of ribbons largely recovered within a month after the noise exposure, although a significant amount of residual damage existed; (2) while the response threshold fully recovered in a month, the temporal processing continued to be deteriorated during this period.
在足以避免永久性阈移的低水平噪声暴露下，已发现其会导致小鼠耳蜗中的螺旋神经节神经元（SGNs）发生大规模、延迟性退化。传入神经支配的损伤是由突触带的丢失引发的，而在小鼠中，这种丢失在很大程度上是不可逆转的。在豚鼠耳蜗中也发现了类似的 SGN 延迟性丢失，但程度较低，这表明 SGN 对噪声的敏感性存在跨物种差异。带突触损伤是“沉默”发生的，即它不会像传统测量那样影响听力阈值，而且这种损伤的功能后果尚不清楚。在本研究中，我们通过关注时间内带计数的动态变化以及由此产生的时间处理变化，进一步探讨了噪声对豚鼠耳蜗传入神经支配的影响。结果发现：(1) 与小鼠的报告相反，尽管仍存在大量残留损伤，但在噪声暴露后一个月内，初始带的丢失大部分得到了恢复；(2) 虽然一个月后反应阈值完全恢复，但在此期间，时间处理仍在恶化。
