Division of Otolaryngology and Program in Neuroscience, University of Utah, 30 North, 1900 East, Salt Lake City, UT 84132-0002, USA.
J Assoc Res Otolaryngol. 2012 Aug;13(4):505-15. doi: 10.1007/s10162-012-0329-0. Epub 2012 Apr 25.
Temporary hearing threshold shift (TTS) resulting from a "benign" noise exposure can cause irreversible auditory nerve afferent terminal damage and retraction. While hearing thresholds and acute tissue injury recover within 1-2 weeks after a noise overexposure, it is not clear if multiple TTS noise exposures would result in cumulative damage even though sufficient TTS recovery time is provided. Here, we tested whether repeated TTS noise exposures affected permanent hearing thresholds and examined how that related to inner ear histopathology. Despite a peak 35-40 dB TTS 24 hours after each noise exposure, a double dose (2 weeks apart) of 100 dB noise (8-16 kHz) exposures to young (4-week-old) CBA mice resulted in no permanent threshold shifts (PTS) and abnormal distortion product otoacoustic emissions (DPOAE). However, although auditory brainstem response (ABR) thresholds recovered fully in once- and twice-exposed animals, the growth function of ABR wave 1( p-p ) amplitude (synchronized spiral ganglion cell activity) was significantly reduced to a similar extent, suggesting that damage resulting from a second dose of the exposure was not proportional to that observed after the initial exposure. Estimate of surviving inner hair cell afferent terminals using immunostaining of presynaptic ribbons revealed ribbon loss of ∼ 40 % at the ∼ 23 kHz region after the first round of noise exposure, but no additional loss of ribbons after the second exposure. In contrast, a third dose of the same noise exposure resulted in not only TTS, but also PTS even in regions where DPOAEs were not affected. The pattern of PTS seen was not entirely tonotopically related to the noise band used. Instead, it resembled more to that of age-related hearing loss, i.e., high frequency hearing impairment towards the base of the cochlea. Interestingly, after a 3rd dose of the noise exposure, additional loss of ribbons (another ≈ 25 %) was observed, suggesting a cumulative detrimental effect from individual "benign" noise exposures, which should result in a significant deficit in central temporal processing.
短暂性听阈移（TTS）是由于“良性”噪声暴露引起的，可能导致不可逆的听神经传入末端损伤和回缩。虽然在噪声过度暴露后 1-2 周内听力阈值和急性组织损伤会恢复，但目前尚不清楚多次 TTS 噪声暴露是否会导致累积性损伤，即使提供了足够的 TTS 恢复时间。在这里，我们测试了重复 TTS 噪声暴露是否会影响永久性听力阈值，并研究了这与内耳组织病理学的关系。尽管每次噪声暴露后 24 小时都会出现 35-40dB 的 TTS，但在年轻（4 周龄）CBA 小鼠中，间隔 2 周两次给予 100dB 噪声（8-16kHz）暴露，不会导致永久性阈移（PTS）和异常畸变产物耳声发射（DPOAE）。然而，尽管一次性和两次暴露的动物的听觉脑干反应（ABR）阈值完全恢复，但 ABR 波 1（p-p）振幅的生长函数（同步螺旋神经节细胞活动）显著降低到相同程度，这表明第二次暴露引起的损伤与初次暴露后观察到的损伤不成比例。使用突触前带免疫染色来估计内毛细胞传入末端的存活情况，结果表明在第一轮噪声暴露后约 23kHz 区域的带丢失了约 40%，但第二次暴露后没有进一步的带丢失。相比之下，在第三次相同噪声暴露后，不仅会出现 TTS，而且会出现 PTS，即使在 DPOAE 不受影响的区域也是如此。观察到的 PTS 模式与噪声频段不完全有关。相反，它更类似于与年龄相关的听力损失，即耳蜗底部高频听力受损。有趣的是，在第三次噪声暴露后，观察到带的额外丢失（另约 25%），这表明来自单个“良性”噪声暴露的累积有害影响，这应该导致中央颞区处理能力的显著缺陷。
