Sleep Deprivation Linked to Cochlear Synaptopathy and Hearing Shifts

Background: Sleep deprivation (SD) is linked to auditory system damage, with over 61.8% of sudden deafness patients experiencing SD. Clinical observations suggest that SD may contribute to conditions like tinnitus and hearing loss, particularly in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), which is known to disrupt sleep quality.

Method: This study utilized a novel curling prevention by water (CPW) paradigm for prolonged SD in mice to create a reliable animal model. Mice were subjected to sleep deprivation for 72 hours and auditory brainstem response (ABR) testing was performed immediately after (D0), and on days 3 (D3) and 7 (D7) post-deprivation to assess changes in auditory function. Additionally, protein expression in cochlear tissues was analyzed using data-independent acquisition proteomics.

Result: During a 72-hour SD period, ABR testing revealed significant increases in hearing thresholds compared to the control group, specifically 13 dB (click), 14 dB (4 kHz), 8 dB (8 kHz), 7 dB (16 kHz), and 31 dB (32 kHz) at D0. On D3, some recovery was noted, though thresholds remained elevated, while at D7, thresholds returned to baseline levels. Proteomic analysis identified 898 differentially expressed proteins, predominantly linked to oxidative stress and inflammatory responses, highlighting the activation of the TLR4/NF-κB/NLRP3 signaling pathway.

Conclusion: This study demonstrates that prolonged SD induces significant temporary auditory impairment through inflammation and oxidative stress mechanisms within the cochlea, indicating the necessity for monitoring auditory health in patients with sleep disorders. Limitations include the focus on acute SD effects and the need for further studies to elucidate the chronic effects of SD on auditory function and explore deeper molecular mechanisms.

Original citation address: https://www.besjournal.com/en/article/doi/10.3967/bes2026.022