Möhrle Dorit, Ni Kun, Varakina Ksenya, Bing Dan, Lee Sze Chim, Zimmermann Ulrike, Knipper Marlies, Rüttiger Lukas
Department of Otolaryngology, Head & Neck Surgery, Tübingen Hearing Research Centre (THRC), Molecular Physiology of Hearing, University of Tübingen, Tübingen, Germany.
Department of Otolaryngology, Head & Neck Surgery, Tübingen Hearing Research Centre (THRC), Molecular Physiology of Hearing, University of Tübingen, Tübingen, Germany; Department of Otolaryngology, Head & Neck Surgery, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Neurobiol Aging. 2016 Aug;44:173-184. doi: 10.1016/j.neurobiolaging.2016.05.001. Epub 2016 May 10.
A dramatic shift in societal demographics will lead to rapid growth in the number of older people with hearing deficits. Poorer performance in suprathreshold speech understanding and temporal processing with age has been previously linked with progressing inner hair cell (IHC) synaptopathy that precedes age-dependent elevation of auditory thresholds. We compared central sound responsiveness after acoustic trauma in young, middle-aged, and older rats. We demonstrate that IHC synaptopathy progresses from middle age onward and hearing threshold becomes elevated from old age onward. Interestingly, middle-aged animals could centrally compensate for the loss of auditory fiber activity through an increase in late auditory brainstem responses (late auditory brainstem response wave) linked to shortening of central response latencies. In contrast, old animals failed to restore central responsiveness, which correlated with reduced temporal resolution in responding to amplitude changes. These findings may suggest that cochlear IHC synaptopathy with age does not necessarily induce temporal auditory coding deficits, as long as the capacity to generate neuronal gain maintains normal sound-induced central amplitudes.
社会人口结构的巨大变化将导致听力有缺陷的老年人数量迅速增长。先前已将随着年龄增长在阈上言语理解和时间处理方面表现较差与先于年龄依赖性听觉阈值升高的进行性内毛细胞（IHC）突触病变联系起来。我们比较了年轻、中年和老年大鼠在声创伤后的中枢声音反应性。我们证明，IHC突触病变从中年开始进展，听力阈值从老年开始升高。有趣的是，中年动物可以通过与缩短中枢反应潜伏期相关的晚期听觉脑干反应（晚期听觉脑干反应波）增加来在中枢补偿听觉纤维活动的丧失。相比之下，老年动物未能恢复中枢反应性，这与对幅度变化反应的时间分辨率降低相关。这些发现可能表明，只要产生神经元增益的能力保持正常的声音诱发中枢振幅，随着年龄增长的耳蜗IHC突触病变不一定会导致时间听觉编码缺陷。
