• Kelly Radziwon, Benjamin D Auerbach, Dalian Ding, Xiaopeng Liu, Guang-Di Chen, and Richard Salvi.
• Center for Hearing and Deafness, SUNY at Buffalo, Buffalo, NY 14214, USA.
• Neuroscience. 2019 Dec 1; 422: 212227212-227.

AbstractNoise-induced hearing loss generally induces loudness recruitment, but sometimes gives rise to hyperacusis, a debilitating condition in which moderate intensity sounds are perceived abnormally loud. In an attempt to develop an animal model of loudness hyperacusis, we exposed rats to a 16-20 kHz noise at 104 dB SPL for 12 weeks. Behavioral reaction time-intensity functions were used to assess loudness growth functions before, during and 2-months post-exposure. During the exposure, loudness recruitment (R) was present in the region of hearing loss, but subtle evidence of hyperacusis (H) started to emerge at the border of the hearing loss. Unexpectedly, robust evidence of hyperacusis appeared below and near the edge of the hearing loss 2-months post-exposure. To identify the neural correlates of hyperacusis and test the central gain model of hyperacusis, we recorded population neural responses from the cochlea, auditory cortex and lateral amygdala 2-months post-exposure. Compared to controls, the neural output of the cochlea was greatly reduced in the noise group. Consistent with central gain models, the gross neural responses from the auditory cortex and amygdala were proportionately much larger than those from the cochlea. However, despite central amplification, the population responses in the auditory cortex and amygdala were still below the level needed to fully account for hyperacusis and/or recruitment. Having developed procedures that can consistently induce hyperacusis in rats, our results set the stage for future studies that seek to identify the neurobiological events that give rise to hyperacusis and to develop new therapies to treat this debilitating condition.Copyright © 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

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