Liberman M Charles, Liberman Leslie D, Maison Stéphane F
Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts, United States of America.
Eaton-Peabody Laboratory, Massachusetts Eye & Ear Infirmary, Boston, Massachusetts, United States of America.
PLoS One. 2015 Nov 18;10(11):e0142341. doi: 10.1371/journal.pone.0142341. eCollection 2015.
Synapses between cochlear nerve terminals and hair cells are the most vulnerable elements in the inner ear in both noise-induced and age-related hearing loss, and this neuropathy is exacerbated in the absence of efferent feedback from the olivocochlear bundle. If age-related loss is dominated by a lifetime of exposure to environmental sounds, reduction of acoustic drive to the inner ear might improve cochlear preservation throughout life. To test this, we removed the tympanic membrane unilaterally in one group of young adult mice, removed the olivocochlear bundle in another group and compared their cochlear function and innervation to age-matched controls one year later. Results showed that tympanic membrane removal, and the associated threshold elevation, was counterproductive: cochlear efferent innervation was dramatically reduced, especially the lateral olivocochlear terminals to the inner hair cell area, and there was a corresponding reduction in the number of cochlear nerve synapses. This loss led to a decrease in the amplitude of the suprathreshold cochlear neural responses. Similar results were seen in two cases with conductive hearing loss due to chronic otitis media. Outer hair cell death was increased only in ears lacking medial olivocochlear innervation following olivocochlear bundle cuts. Results suggest the novel ideas that 1) the olivocochlear efferent pathway has a dramatic use-dependent plasticity even in the adult ear and 2) a component of the lingering auditory processing disorder seen in humans after persistent middle-ear infections is cochlear in origin.
在噪声性和年龄相关性听力损失中,耳蜗神经末梢与毛细胞之间的突触是内耳中最脆弱的部分,并且在缺乏橄榄耳蜗束的传出反馈时,这种神经病变会加剧。如果年龄相关性听力损失主要是由一生暴露于环境声音所致,那么减少传入内耳的声驱动可能会在一生中改善耳蜗的保护。为了验证这一点,我们在一组年轻成年小鼠中单侧摘除鼓膜,在另一组中切断橄榄耳蜗束,并在一年后将它们的耳蜗功能和神经支配与年龄匹配的对照组进行比较。结果显示,摘除鼓膜以及随之而来的阈值升高产生了适得其反的效果:耳蜗传出神经支配显著减少,尤其是到内毛细胞区域的外侧橄榄耳蜗末梢,并且耳蜗神经突触数量相应减少。这种损失导致阈上耳蜗神经反应的幅度降低。在两例因慢性中耳炎导致传导性听力损失的病例中也观察到了类似结果。仅在切断橄榄耳蜗束后缺乏内侧橄榄耳蜗神经支配的耳中,外毛细胞死亡增加。结果提示了两个新观点:1)即使在成年耳中,橄榄耳蜗传出通路也具有显著的使用依赖性可塑性;2)人类在持续性中耳感染后出现的持续性听觉加工障碍的一部分起源于耳蜗。