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
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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.

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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。
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来源期刊
Acta Oto-Laryngologica
Acta Oto-Laryngologica 医学-耳鼻喉科学
CiteScore
2.50
自引率
0.00%
发文量
99
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.
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