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 26
TA  - eneuro
PG  - ENEURO.0250-18.2018
4099  - http://www.eneuro.org/content/early/2018/07/26/ENEURO.0250-18.2018.short
4100  - http://www.eneuro.org/content/early/2018/07/26/ENEURO.0250-18.2018.full
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), 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 hyper-reactive 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.Significance Statement Noise exposure can cause significant damage to the peripheral auditory system. Previous work has shown that the dorsal cochlear nucleus, inferior colliculus, auditory thalamus, and auditory cortex become hyperactive following damage to the peripheral auditory system, which may compensate for decreased sensory input. Here we show that after noise exposure, hyperactivity develops in the auditory brainstem as a result of reorganization of excitation and inhibition in the ventral cochlear nucleus. The compensatory plasticity observed at this early stage of the primary auditory pathway may contribute to the hyperactivity reported at later stages. Further, we show that this hyperactivity can compensate for reduced sensory input to partially restore some aspects of auditory function.