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噪声性耳蜗突触病变和隐匿性听力损失的后果及机制,重点关注噪声中的信号感知和时间处理

Consequences and Mechanisms of Noise-Induced Cochlear Synaptopathy and Hidden Hearing Loss, With Focuses on Signal Perception in Noise and Temporal Processing.

作者信息

Wang Hui, Aiken Steven J, Wang Jian

机构信息

Shanghai Key Laboratory of Sleep Disordered Breathing, Department of Orolaryngology-Head and Neck Surgery, Otolaryngology Institute of Shanghai Jiao Tong University, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, P. R. China.

School of Communication Sciences and Disorders, Dalhousie University, Halifax, NS, Canada.

出版信息

Adv Sci (Weinh). 2025 Aug;12(29):e2409322. doi: 10.1002/advs.202409322. Epub 2025 Apr 7.

Abstract

Noise-induced synaptopathy and relevant hidden hearing loss (NIS and NIHHL) have been a hot topic in hearing research for almost 15 years. The progress is summarized in this review to address the reversibility of the synaptic damage after the initial loss, and the role of functional deficit in the repaired synapses as the reason for hearing impairment in addition to the deafferentiation caused by the synaptic loss, per se. The evidence supporting the synaptic repair is summarized. It is pointed out that coding-in-noise deficit (CIND) may not be the major problem of NIS and NIHHL, since solid evidence supporting the existence of this deficit is not available even in animal studies, as well as in in human reports. Rather, temporal processing deficits are clearly demonstrated in subjects with NIS and potentially NIHHL. The idea of CIND as the major concern in NIHHL is proposed based upon the functional categorization of the auditory nerve (ANF) by spontaneous rate and the biased loss of the ribbon synapses innervation the low-SR ANF. The limitation of this hypothesis is discussed in detail. The review also addresses the difficulty of translating animal data to humans and the need for new research in the future.

摘要

近15年来,噪声性突触病变及相关隐匿性听力损失(NIS和NIHHL)一直是听力研究中的热点话题。本综述总结了相关进展,以探讨初始损伤后突触损伤的可逆性,以及除突触损失本身导致的去传入作用外,修复后突触中的功能缺陷作为听力障碍原因的作用。总结了支持突触修复的证据。指出噪声编码缺陷(CIND)可能不是NIS和NIHHL的主要问题,因为即使在动物研究以及人类报告中,也没有确凿证据支持这种缺陷的存在。相反,在患有NIS以及可能患有NIHHL的受试者中,明显存在时间处理缺陷。基于听觉神经(ANF)的自发放电率功能分类以及低自发放电率ANF的带状突触支配的偏向性损失,提出了CIND是NIHHL主要问题的观点。详细讨论了这一假设的局限性。本综述还探讨了将动物数据转化为人类数据的困难以及未来新研究工作的必要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80fc/12362826/303137480d45/ADVS-12-2409322-g007.jpg

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