The quantification and mRNA expression levels of cochlear synapses in C57BL/6j mice following repeated exposure to noise.

IF 1.2 4区医学 Q3 OTORHINOLARYNGOLOGY

Acta Oto-Laryngologica Pub Date : 2024-10-01 Epub Date: 2024-10-21 DOI:10.1080/00016489.2024.2413385

Minfei Qian, Zhuowei Yao, Qixuan Wang, Yaqi Zhou, Zhiwu Huang, Jiping Li

{"title":"The quantification and mRNA expression levels of cochlear synapses in C57BL/6j mice following repeated exposure to noise.","authors":"Minfei Qian, Zhuowei Yao, Qixuan Wang, Yaqi Zhou, Zhiwu Huang, Jiping Li","doi":"10.1080/00016489.2024.2413385","DOIUrl":null,"url":null,"abstract":"Background: Noise-induced cochlear synaptopathy has recently emerged as a focus in hearing research.Purpose: This study aimed to examine the impact of repeated noise exposure on the quantification and mRNA expression levels of cochlear synapses.Methods: Measurements were conducted at baseline, 1 day, and 14 days post-exposure to 88 or 97 dB SPL noise (2 h/day for 7 days, frequency range 2-20 kHz). Auditory brainstem responses (ABRs), immunofluorescence and quantitative real-time PCR (qRT-PCR) were used to examine the results.Results: 1. Exposure to 88 dB SPL caused minimal changes in ABRs, ribbon morphology and medial olivocochlear (MOC) efferent synapses; elevation of synaptophysin(SYP) and α9α10 nAchR mRNA levels were observed. 2. Exposure to 97 dB SPL caused threshold shift and synaptopathy of ribbon and MOC; downregulation of α10nAchR, SYP and ctbp2 mRNA levels were observed.Conclusion: Noise-induced cochlear synaptic degeneration involves both afferent and efferent synaptopathy.","PeriodicalId":6880,"journal":{"name":"Acta Oto-Laryngologica","volume":" ","pages":"558-564"},"PeriodicalIF":1.2000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Oto-Laryngologica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/00016489.2024.2413385","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/21 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"OTORHINOLARYNGOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Noise-induced cochlear synaptopathy has recently emerged as a focus in hearing research.

Purpose: This study aimed to examine the impact of repeated noise exposure on the quantification and mRNA expression levels of cochlear synapses.

Methods: Measurements were conducted at baseline, 1 day, and 14 days post-exposure to 88 or 97 dB SPL noise (2 h/day for 7 days, frequency range 2-20 kHz). Auditory brainstem responses (ABRs), immunofluorescence and quantitative real-time PCR (qRT-PCR) were used to examine the results.

Results: 1. Exposure to 88 dB SPL caused minimal changes in ABRs, ribbon morphology and medial olivocochlear (MOC) efferent synapses; elevation of synaptophysin(SYP) and α9α10 nAchR mRNA levels were observed. 2. Exposure to 97 dB SPL caused threshold shift and synaptopathy of ribbon and MOC; downregulation of α10nAchR, SYP and ctbp2 mRNA levels were observed.

Conclusion: Noise-induced cochlear synaptic degeneration involves both afferent and efferent synaptopathy.

查看原文本刊更多论文

反复暴露于噪声后 C57BL/6j 小鼠耳蜗突触的定量和 mRNA 表达水平。

目的：本研究旨在探讨反复暴露于噪声对耳蜗突触的定量和 mRNA 表达水平的影响：在暴露于 88 或 97 dB SPL 噪声（每天 2 小时，持续 7 天，频率范围 2-20 kHz）后的基线、1 天和 14 天进行测量。使用听觉脑干反应（ABRs）、免疫荧光和定量实时 PCR（qRT-PCR）来检测结果：1.1. 暴露于 88 dB SPL 对 ABRs、色带形态和内侧橄榄耳（MOC）传出突触的影响极小；观察到突触素（SYP）和 α9α10 nAchR mRNA 水平的升高。2.2. 暴露于 97 dB SPL 会导致阈值偏移以及带状突触和 MOC 的突触病变；观察到 α10nAchR、SYP 和 ctbp2 mRNA 水平下调：结论：噪声诱导的耳蜗突触变性涉及传入和传出突触病变。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Acta Oto-Laryngologica 医学-耳鼻喉科学

CiteScore

2.50

自引率

0.00%

发文量

审稿时长

3-6 weeks

期刊介绍： Acta Oto-Laryngologica is a truly international journal for translational otolaryngology and head- and neck surgery. The journal presents cutting-edge papers on clinical practice, clinical research and basic sciences. Acta also bridges the gap between clinical and basic research.