Noise-Induced loudness recruitment and hyperacusis: Insufficient central gain in auditory cortex and amygdala. (1st December 2019)

• Record Type: Journal Article
• Authors: Radziwon, Kelly; Auerbach, Benjamin D.; Ding, Dalian; Liu, Xiaopeng; Chen, Guang-Di; Salvi, Richard
• Is Part Of: Neuroscience. Volume 422(2019)
• Page Start: 212
• Page End: 227
• Publication Date: 2019-12-01
• Subjects: AAF anterior auditory field -- AC auditory cortex -- CAP compound action potential -- dB deciBel -- IHC inner hair cell -- I/O input/output -- LA lateral amygdala -- MGB medial geniculate body -- MUC multiunit clusters -- NBN narrowband noise -- OHC outer hair cell -- PSTH peristimulus time histogram -- RT reaction time -- RT-I reaction time-intensity -- SEM standard error of the mean -- SPL sound pressure level -- VAF ventral auditory field; Loudness recruitment -- Hyperacusis -- Central gain -- Noise exposure -- Auditory cortex -- Amygdala; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2019.09.010
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: Loudness recruitment emerged during prolonged exposure to intense high frequency noise. Hyperacusis-like behavior appeared below and near the edge of the high frequency hearing loss 2-months post-exposure. The neural output of the cochlea was greatly reduced after the noise exposure. Neural responses in auditory cortex and amygdala were much larger than the cochlea, but insufficient to explain hyperacusis. Abstract: Noise-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.