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慢性应激导致的耳鸣产生及行为变化：大鼠模型的行为与脑研究

Tinnitus Generation and Behavioral Changes Caused by Chronic Stress: A Behavioral and Brain Study in a Rat Model.

作者信息

Kim Ye Lin, Yu Hyo Jeong, Kim Min Jung, Han Jae Sang, Lim Ji Hyung, Park So Young, Park Ilyong, Park Shi Nae

机构信息

Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.

Department of Medical Sciences, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.

出版信息

Laryngoscope. 2025 Feb;135(2):873-881. doi: 10.1002/lary.31779. Epub 2024 Oct 16.

DOI:10.1002/lary.31779
PMID:39411919
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11725682/
Abstract

OBJECTIVES

This study explores the connection between chronic stress and tinnitus, a phantom auditory perception, using an animal model.

METHODS

Rats were subjected to 2 h of daily restraint stress for 10 days. Tinnitus was assessed on the last day of stress exposure using the gap response of pre-pulse inhibition acoustic reflex, measured at 60 dB background sound level at 8, 16, and 20 kHz. Chronic stress-exposed rats were categorized into two groups: tinnitus (RTG) and non-tinnitus (RNTG). Various tests, including hearing assessments (distortion product otoacoustic emissions and auditory brainstem response), behavioral evaluations (elevated plus maze test and forced swimming test), and immunohistochemical studies in the auditory and limbic brain regions, were conducted to understand the relationship between chronic stress, tinnitus, and behavioral changes.

RESULTS

Following chronic restraint stress, 64.3% of the rats exhibited tinnitus with no audiometric changes. EPM and FST indicated an increase of anxiety- and depression-related behavior in RTG. Immunohistochemical analyses identified specific alterations in the expression of neurotransmitter receptors within brain regions implicated in tinnitus. Specifically, we observed a decrease in γ-aminobutyric acid A receptor α1 expression and an increase in glutamate receptor (N-methyl-D-aspartate receptor subunit 1 and receptor subunit 2B) expression in specific brain region. These changes suggest a reorganization of neural circuits associated with the tinnitus generation and behavioral changes of the rats after chronic stress exposure.

CONCLUSION

Chronic stress alone can be a causal factor for the generation of tinnitus and behavioral changes through altered neural activities in tinnitus-related brain networks.

LEVEL OF EVIDENCE

NA Laryngoscope, 135:873-881, 2025.

摘要

目的

本研究使用动物模型探讨慢性应激与耳鸣（一种幻听）之间的联系。

方法

大鼠连续10天每天接受2小时的束缚应激。在应激暴露的最后一天，使用预脉冲抑制听觉反射的间隙反应评估耳鸣，在8、16和20kHz的60dB背景声水平下进行测量。慢性应激暴露的大鼠分为两组：耳鸣组（RTG）和非耳鸣组（RNTG）。进行了各种测试，包括听力评估（畸变产物耳声发射和听觉脑干反应）、行为评估（高架十字迷宫试验和强迫游泳试验）以及听觉和边缘脑区的免疫组织化学研究，以了解慢性应激、耳鸣和行为变化之间的关系。

结果

在慢性束缚应激后，64.3%的大鼠出现耳鸣且听力测定无变化。高架十字迷宫试验和强迫游泳试验表明，耳鸣组焦虑和抑郁相关行为增加。免疫组织化学分析确定了耳鸣相关脑区内神经递质受体表达的特定改变。具体而言，我们观察到特定脑区中γ-氨基丁酸A受体α1表达减少，谷氨酸受体（N-甲基-D-天冬氨酸受体亚基1和受体亚基2B）表达增加。这些变化表明，慢性应激暴露后，与大鼠耳鸣产生和行为变化相关的神经回路发生了重组。

结论

单独的慢性应激可能是通过耳鸣相关脑网络中神经活动的改变导致耳鸣产生和行为变化的一个因果因素。

证据水平

NA 喉镜，135:873 - 881，2025年。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c0e/11725682/2f99a0d83f34/LARY-135-873-g005.jpg
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