Speaker
Description
Hyperacusis affects 2-15% of the population, causing painful sensitivity to everyday sounds, yet its pathophysiology remains obscure due to limited animal models and frequent tinnitus comorbidity. This study aimed to identify neural biomarkers and behavioral changes reliably characterizing hyperacusis.Mice were exposed to acoustic trauma (2h, 95 dB SPL) inducing temporary hearing loss. Behavioral and electrophysiological assessments were conducted in awake animals pre- and post-trauma. Noise exposure increased startle reflex amplitude (hyperacusis correlate) and decreased gap inhibition (tinnitus correlate) in subsets of animals. Phenotypic scales revealed positive correlations between hyperacusis severity and evoked response amplitude in the inferior colliculus and auditory cortex 5-10 weeks post-exposure. No such correlation existed for tinnitus, and spontaneous EEG remained unchanged. Crucially, startle reflex amplitude correlated with central auditory evoked responses despite recovered peripheral thresholds.We successfully identified a hyperacusis phenotype based on simultaneous behavioral and neural response enhancements. These findings elucidate pathophysiological mechanisms impacting the central auditory system following noise overexposure, independent of permanent hearing loss, paving the way for targeted treatments.