Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms.
Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms.
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DOI：
10.1016/j.heares.2017.01.003
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发表时间：
2017-06
期刊：
影响因子：
2.8
通讯作者：
Kujawa SG
中科院分区：
文献类型：
--
作者：
Liberman MC;Kujawa SG
人类听力损失的常见原因——暴露于噪音或耳毒性药物以及衰老——通常会损害感觉毛细胞，这在临床听力图上表现为阈值升高。然而，最近对动物模型的研究表明，早在这种明显的听力损失出现之前，一种更隐蔽但可能更常见的过程正在发生，该过程永久中断感觉内毛细胞和耳蜗神经纤维亚群之间的突触通讯。受影响的神经元的沉默会改变听觉信息处理，无论是否伴有阈值升高，并且可能导致各种感知异常，包括噪声中言语困难、耳鸣和听觉过敏。这里描述的工作将回顾这种耳蜗突触病的结构和功能表现，并将考虑其在耳朵中出现和进展的可能机制，无论是否存在由人类几种常见原因引起的传统“听力损失”。
Common causes of hearing loss in humans - exposure to loud noise or ototoxic drugs and aging - often damage sensory hair cells, reflected as elevated thresholds on the clinical audiogram. Recent studies in animal models suggest, however, that well before this overt hearing loss can be seen, a more insidious, but likely more common, process is taking place that permanently interrupts synaptic communication between sensory inner hair cells and subsets of cochlear nerve fibers. The silencing of affected neurons alters auditory information processing, whether accompanied by threshold elevations or not, and is a likely contributor to a variety of perceptual abnormalities, including speech-in-noise difficulties, tinnitus and hyperacusis. Work described here will review structural and functional manifestations of this cochlear synaptopathy and will consider possible mechanisms underlying its appearance and progression in ears with and without traditional ‘hearing loss’ arising from several common causes in humans.