Acceleration of age-related hearing loss by early noise exposure: Evidence of a misspent youth
Acceleration of age-related hearing loss by early noise exposure: Evidence of a misspent youth
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DOI：
10.1523/jneurosci.4985-05.2006
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发表时间：
2006-02-15
影响因子：
5.3
通讯作者：
Liberman, MC
中科院分区：
文献类型：
--
作者：
Kujawa, SG;Liberman, MC
人类中与噪音相关的听力损失和噪声引起的听力损失是多因素的，其中有许多变量的贡献和潜在的相互作用，这些变量可以影响最终结果。最近的一项回顾性临床研究表明，年龄-噪声相互作用加剧了先前噪声损伤耳朵中与年龄相关的听力损失（Gates等人，2000）。在这里，我们通过比较CBA/CaJ小鼠暴露相同（8-16 kHz噪声带，100 dB声压水平2小时）但不同年龄（4-124周）的噪声诱导和年龄相关性听力损失（NIHL;阿勒），并与未暴露的队列保持不同的暴露后时间（2-96周），在动物模型中解决了这个问题。当暴露后2周进行评估时，暴露于辐射的动物（4-8周）的最大阈值变化为40-50 dB;暴露于辐射的老年动物（>= 16周）在相同的暴露后时间基本上没有变化。然而，当长时间暴露后，之前暴露过的动物表现出阿勒和组织病理学，与未暴露的、衰老的动物或仅暴露2周的老年动物根本不同。具体而言，他们表现出大量的，持续恶化的耳蜗神经反应，没有额外的变化，前神经反应，和相应的组织学证据的原发性神经变性整个耳蜗。这对于暴露于噪声的动物尤其如此;然而，在暴露后96周的所有暴露于噪声的动物中观察到迟发性神经病，即使是暴露后2周未显示NIHL的动物。数据表明，早期噪声暴露引起的病理性但亚致死性的变化使内耳明显更容易衰老。
Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8-16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4-124 weeks) and held with unexposed cohorts for different postexposure times (2-96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4-8 weeks) were 40-50 dB; older-exposed animals (>= 16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.