UC Riverside

Noise-induced hearing loss (NIHL) is a major cause of auditory processing impairment and major cognitive impairment. Peripherally, cochlear hair cell damage has been studied extensively in NIHL. Fewer studies have looked at effects more centrally, but these studies have led to the emerging theory of ‘central gain’. The lack of peripheral input (deafferentation) following NIHL increases gain in central auditory regions, leading to exaggerated spontaneous and sound evoked responses. These responses may lead to tinnitus and hyperacusis, for which currently there are no treatment to reduce these comorbidities following NIHL. The cellular mechanisms underlying the increased gain is unclear, however we hypothesize that neuroinflammation and matrix-metalloproteinase-9 (MMP-9) are upregulated following NIHL causing disruption in population level activity ultimately leading to enhanced central gain and temporal processing. To address this gap, we designed a series of experiments to identify the effects of NIHL in the brain. We have made several key findings. Firstly, there is a cortical-region specific difference in temporal processing, but not in sound detection and recovery following NIHL. Second, MMP-9 activity is not upregulated at 1-day post-NIHL. Last, minocycline enhances sound detection amplification after temporary hearing loss, but does not affect temporal processing or auditory brainstem thresholds. Our data provides insight into longitudinal modulations of sound detection and temporal processing in auditory cortical regions with potential timecourse and therapeutic targets.