Examines metabolic and vascular changes in mouse amygdala following acute acoustic trauma, suggesting significant non-auditory brain effects.
Acute noise exposure induces hearing threshold shifts and potentially affects the amygdala, yet the associated metabolic and vascular alterations remain unclear. This study examined the immediate and short-term effects of a single acute noise exposure (100 dB SPL, 2 h) on metabolic activity, hemodynamics, and vascular structure in the mouse amygdala. Untargeted metabolomics and ultrasound localization microscopy were used to profile amygdala tissues and assess local blood flow velocity and vascular density before exposure and at 1 and 7 days post-exposure. Results showed elevated auditory thresholds across all frequencies at day 1, with partial recovery at select frequencies by day 7. Metabolomics revealed significantly increased glutamate levels that persisted through day 7, while GABA levels decreased at day 1 and returned to baseline by day 7, indicating an excitation–inhibition imbalance. Moreover, amygdala blood flow velocity increased significantly by day 1 and remained elevated at day 7, accompanied by a marked increase in vascular density by day 7. This study provides systematic evidence that acute noise exposure induces metabolic disturbances, hemodynamic changes, and vascular changes in the amygdala, offering new insights into the direct impact of noise on non-auditory brain regions.
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Tan et al. (2026) studied this question.
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