Efferent feedback minimizes cochlear neuropathy from moderate noise exposure.
Efferent feedback minimizes cochlear neuropathy from moderate noise exposure.
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DOI：
10.1523/jneurosci.5027-12.2013
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发表时间：
2013-03-27
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影响因子：
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通讯作者：
Liberman MC
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文献类型：
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作者：
Maison SF;Usubuchi H;Liberman MC
虽然耳蜗传出反馈通路的保护作用已被充分记录，但先前的工作集中在毛细胞损伤和耳蜗阈值升高，以及相应地产生它们所需的高声压级（> 100 dB SPL）上。在这里，我们探讨了噪声引起的耳蜗神经元的损失，发生在较低强度的曝光和永久性阈值偏移的情况下。使用共聚焦显微镜计数毛细胞和耳蜗神经纤维之间的突触，并使用听觉脑干反应和耳声发射的测量，以评估耳蜗突触前和突触后功能，我们比较了从一个星期暴露于中等水平的噪声（84 dB SPL）在小鼠不同程度的耳蜗de-efferentations由手术损伤橄榄耳蜗通路诱导的损害。这样的暴露导致最小的急性阈值偏移，而在具有正常传出反馈的小鼠中没有慢性偏移。在去传出神经的动物中，耳蜗神经突触的损失高达40%，听觉脑干反应的振幅也相应下降。定量分析的de-efferentation内与外毛细胞区表明，外毛细胞传出是最重要的，在尽量减少这种神经病变，大概是凭借他们的声音诱发的反馈减少耳蜗放大。这种声音过度的温和性质表明，即使在日常的声学环境中，耳蜗神经元也处于危险之中，因此，在设计这种反馈通路时，对耳蜗保护的需要似乎是一种驱动力。
Although protective effects of the cochlea’s efferent feedback pathways have been well documented, prior work has focused on hair cell damage and cochlear threshold elevation and, correspondingly, on the high sound pressure levels (> 100 dB SPL) necessary to produce them. Here we explore the noise-induced loss of cochlear neurons that occurs with lower intensity exposures and in the absence of permanent threshold shifts. Using confocal microscopy to count synapses between hair cells and cochlear nerve fibers, and using measurement of auditory brainstem responses and otoacoustic emissions to assess cochlear pre- and post-synaptic function, we compare the damage from a weeklong exposure to moderate-level noise (84 dB SPL) in mice with varying degrees of cochlear de-efferentation induced by surgical lesion to the olivocochlear pathway. Such exposure causes minimal acute threshold shift and no chronic shifts in mice with normal efferent feedback. In de-efferented animals, there was up to 40% loss of cochlear nerve synapses and a corresponding decline in the amplitude of the auditory brainstem response. Quantitative analysis of the de-efferentation in inner vs. outer hair cell areas suggested that outer hair cell efferents are most important in minimizing this neuropathy, presumably by virtue of their sound-evoked feedback reduction of cochlear amplification. The moderate nature of this acoustic overexposure suggests that cochlear neurons are at risk even in everyday acoustic environments, and, thus, that the need for cochlear protection is plausible as a driving force in the design of this feedback pathway.