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获得性感音神经性听力损失中的耳蜗突触病变:表现与机制

Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms.

作者信息

Liberman M Charles, Kujawa Sharon G

机构信息

Department of Otology and Laryngology, Harvard Medical School, Boston MA, USA; Eaton-Peabody Laboratories, Massachusetts Eye & Ear Infirmary, Boston MA, USA.

Department of Otology and Laryngology, Harvard Medical School, Boston MA, USA; Eaton-Peabody Laboratories, Massachusetts Eye & Ear Infirmary, Boston MA, USA.

出版信息

Hear Res. 2017 Jun;349:138-147. doi: 10.1016/j.heares.2017.01.003. Epub 2017 Jan 10.

Abstract

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.

摘要

人类听力损失的常见原因——接触高强度噪音、使用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,最近在动物模型中的研究表明,在明显的听力损失出现之前,一个更隐匿但可能更常见的过程正在发生,这个过程会永久性地中断感觉性内毛细胞与耳蜗神经纤维亚群之间的突触通讯。受影响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,并且很可能是导致各种感知异常的原因,包括噪声环境下言语理解困难、耳鸣和听觉过敏。本文所述的工作将回顾这种耳蜗突触病变的结构和功能表现,并探讨在有或没有因人类几种常见原因引起的传统“听力损失”的耳朵中,其出现和进展的潜在机制。

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引用本文的文献

本文引用的文献

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Toward a Differential Diagnosis of Hidden Hearing Loss in Humans.迈向人类隐匿性听力损失的鉴别诊断
PLoS One. 2016 Sep 12;11(9):e0162726. doi: 10.1371/journal.pone.0162726. eCollection 2016.

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