Immediate and delayed cochlear neuropathy after noise exposure in pubescent mice.
Immediate and delayed cochlear neuropathy after noise exposure in pubescent mice.
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DOI：
10.1371/journal.pone.0125160
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Stankovic KM
中科院分区：
文献类型：
--
作者：
Jensen JB;Lysaght AC;Liberman MC;Qvortrup K;Stankovic KM
成年啮齿类动物中的中度听觉过度暴露已知会导致感觉内毛细胞（IHC）上的突触的急性丧失和听神经的延迟变性，尽管完全可逆的暂时性阈值偏移（TTS）和形态学上完整的毛细胞。我们的目的是确定是否耳蜗突触病神经病变后发生噪声暴露在青春期，并定义神经性与非神经性噪声水平青春期小鼠。当将6周龄CBA/CaJ小鼠暴露于8-16 kHz带通噪声2小时时，我们将97 dB声压级（SPL）定义为与TTS相关的这种特定类型的神经性暴露的阈值，并且将94 dB SPL定义为与TTS相关的最高非神经性噪声水平。暴露于100 dB SPL导致永久性阈值偏移，尽管据报道16周龄小鼠暴露于相同噪声仅导致TTS。听觉脑干反应，这反映了耳蜗神经的总活动的波I的振幅，补充了使用共聚焦显微镜在IHC的突触带计数，并从24小时至16个月后暴露的耳蜗神经的外周轴突和细胞体视学计数。暴露于神经性噪声的小鼠在暴露后24小时表现出立即的耳蜗突触病，并且在暴露后8个月表现出以轴突回缩为特征的延迟的神经变性，并且在暴露后8-16个月表现出螺旋神经节细胞损失。虽然损伤最初仅限于耳蜗基底，但在暴露后8个月，其进展也涉及耳蜗尖。我们的数据表明，神经性和非神经性噪声水平之间的细线与TTS在青春期耳蜗。
Moderate acoustic overexposure in adult rodents is known to cause acute loss of synapses on sensory inner hair cells (IHCs) and delayed degeneration of the auditory nerve, despite the completely reversible temporary threshold shift (TTS) and morphologically intact hair cells. Our objective was to determine whether a cochlear synaptopathy followed by neuropathy occurs after noise exposure in pubescence, and to define neuropathic versus non-neuropathic noise levels for pubescent mice. While exposing 6 week old CBA/CaJ mice to 8-16 kHz bandpass noise for 2 hrs, we defined 97 dB sound pressure level (SPL) as the threshold for this particular type of neuropathic exposure associated with TTS, and 94 dB SPL as the highest non-neuropathic noise level associated with TTS. Exposure to 100 dB SPL caused permanent threshold shift although exposure of 16 week old mice to the same noise is reported to cause only TTS. Amplitude of wave I of the auditory brainstem response, which reflects the summed activity of the cochlear nerve, was complemented by synaptic ribbon counts in IHCs using confocal microscopy, and by stereological counts of peripheral axons and cell bodies of the cochlear nerve from 24 hours to 16 months post exposure. Mice exposed to neuropathic noise demonstrated immediate cochlear synaptopathy by 24 hours post exposure, and delayed neurodegeneration characterized by axonal retraction at 8 months, and spiral ganglion cell loss at 8-16 months post exposure. Although the damage was initially limited to the cochlear base, it progressed to also involve the cochlear apex by 8 months post exposure. Our data demonstrate a fine line between neuropathic and non-neuropathic noise levels associated with TTS in the pubescent cochlea.
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