Characterization of Anxiety-Like Behaviors and Neural Circuitry following Chronic Moderate Noise Exposure in Mice.
| Autor: | Xiaoqi Peng1, Yunfeng Mao1, Yingju Tai1, Bin Luo2,3, Qian Dai4, Xiyang Wang4, Hao Wang4, Yue Liang5, Ruirui Guan5, Chunhua Liu6, Yiping Guo6, Lin Chen2, Zhi Zhang1 zhizhang@ustc.edu.cn, Haitao Wang1,4 |
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| Předmět: |
*Animal experimentation
*Environmental health Statistics Auditory evoked response Hearing Neural pathways In vivo studies Analysis of variance Noise Immunohistochemistry Mann Whitney U Test Stereotaxic techniques T-test (Statistics) Psychometrics Research funding Descriptive statistics Anxiety Data analysis software Data analysis Amygdaloid body Optogenetics Mice Brain stem Auditory cortex Psychological stress Psychosocial factors |
| Zdroj: | Environmental Health Perspectives. Oct2023, Vol. 131 Issue 10, p107004-1-107004-15. 15p. 6 Graphs. |
| Abstrakt: | BACKGROUND: Commonly encountered nontraumatic, moderate noise is increasingly implicated in anxiety; however, the neural substrates underlying this process remain unclear. OBJECTIVES: We investigated the neural circuit mechanism through which chronic exposure to moderate-level noise causes anxiety-like behaviors. METHODS: Mice were exposed to chronic, moderate white noise [85 decibel (dB) sound pressure level (SPL)], 4 h/d for 4 wk to induce anxiety-like behaviors, which were assessed by open field, elevated plus maze, light-dark box, and social interaction tests. Viral tracing, immunofluorescence confocal imaging, and brain slice patch-clamp recordings were used to characterize projections from auditory brain regions to the lateral amygdala. Neuronal activities were characterized by in vivo multielectrode and fiber photometry recordings in awake mice. Optogenetics and chemogenetics were used to manipulate specific neural circuitry. RESULTS: Mice chronically (4 wk) exposed to moderate noise (85 dB SPL, 4 h/d) demonstrated greater neuronal activity in the lateral amygdala (LA), and the LA played a critical role in noise-induced anxiety-like behavior in these model mice. Viral tracing showed that the LA received monosynaptic projections from the medial geniculate body (MG) and auditory cortex (ACx). Optogenetic excitation of the MG → LA or ACx → LA circuits acutely evoked anxiety-like behaviors, whereas their chemogenetic inactivation abolished noise-induced anxiety-like behavior. Moreover, mice chronically exposed to moderate noise were more susceptible to acute stress, with more neuronal firing in the LA, even after noise withdrawal. DISCUSSION: Mice exposed to 4 wk of moderate noise (85 dB SPL, 4 h/d) demonstrated behavioral and physiological differences compared to controls. The neural circuit mechanisms involved greater excitation from glutamatergic neurons of the MG and ACx to LA neurons under chronic, moderate noise exposure, which ultimately promoted anxiety-like behaviors. Our findings support the hypothesis that nontraumatic noise pollution is a potentially serious but unrecognized public health concern. [ABSTRACT FROM AUTHOR] |
| Databáze: | GreenFILE |
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