PT - JOURNAL ARTICLE AU - Katrina M. Schrode AU - Michael A. Muniak AU - Ye-Hyun Kim AU - Amanda M. Lauer TI - Central Compensation in Auditory Brainstem after Damaging Noise Exposure AID - 10.1523/ENEURO.0250-18.2018 DP - 2018 Jul 01 TA - eneuro PG - ENEURO.0250-18.2018 VI - 5 IP - 4 4099 - http://www.eneuro.org/content/5/4/ENEURO.0250-18.2018.short 4100 - http://www.eneuro.org/content/5/4/ENEURO.0250-18.2018.full SO - eNeuro2018 Jul 01; 5 AB - Noise exposure is one of the most common causes of hearing loss and peripheral damage to the auditory system. A growing literature suggests that the auditory system can compensate for peripheral loss through increased central neural activity. The current study sought to investigate the link between noise exposure, increases in central gain, synaptic reorganization, and auditory function. All axons of the auditory nerve project to the cochlear nucleus, making it a requisite nucleus for sound detection. As the first synapse in the central auditory system, the cochlear nucleus is well positioned to respond plastically to loss of peripheral input. To investigate noise-induced compensation in the central auditory system, we measured auditory brainstem responses (ABRs) and auditory perception and collected tissue from mice exposed to broadband noise. Noise-exposed mice showed elevated ABR thresholds, reduced ABR wave 1 amplitudes, and spiral ganglion neuron loss. Despite peripheral damage, noise-exposed mice were hyperreactive to loud sounds and showed nearly normal behavioral sound detection thresholds. Ratios of late ABR peaks (2–4) relative to the first ABR peak indicated that brainstem pathways were hyperactive in noise-exposed mice, while anatomical analysis indicated there was an imbalance between expression of excitatory and inhibitory proteins in the ventral cochlear nucleus. The results of the current study suggest that a reorganization of excitation and inhibition in the ventral cochlear nucleus may drive hyperactivity in the central auditory system. This increase in central gain can compensate for peripheral loss to restore some aspects of auditory function.