Sleep recovers prior to hearing after a single high-intensity noise exposure in mice.

Abstract

The acute effects of a single noise event on sleep and its recovery dynamics remain poorly understood. This study established mouse models of acute noise exposure using single 2-hour sessions of moderate- (80 dB SPL) or high-intensity (100 dB SPL) octave-band noise (8-16 kHz). Auditory brainstem response (ABR) thresholds and 24-hour polysomnography were assessed serially to evaluate the impact on hearing and sleep architecture, as well as their temporal recovery. Exposure to 80 dB SPL noise produced no significant threshold shifts or sleep disturbances 2 days later. In contrast, 100 dB SPL exposure induced substantial auditory threshold elevations across tested frequencies (8-32 kHz) and pronounced sleep disruption at 4 days, characterized by increased wakefulness and reduced non-rapid eye movement (NREM) sleep, while rapid eye movement (REM) sleep remained unaffected. By day 10 post-exposure, sleep architecture had fully recovered to baseline levels, whereas auditory thresholds remained partially elevated, with complete recovery observed only after 3 weeks. Furthermore, c-Fos immunohistochemistry revealed sustained neuronal activation in the inferior colliculus following high-intensity noise exposure, providing a potential neural correlate for the observed sleep disturbance. These findings reveal a clear dissociation in recovery timelines with sleep normalizes prior to the full restoration of auditory function.