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REVIEW PAPER
REVIEW: HYPERACUSIS, ANIMAL MODELS, CHRONIC STRESS, AND AUTISM IN FRAGILE X
1
Departmen of Communication Disorders and Sciences, University of Central Florida, Orlando, United States
2
Department of Radiology, Nanjing First Hospital, Nanjing Medical University, China
3
School of Molecular and Cellular Biology, University of Illinois at Urbana-Champaign, United States
A - Research concept and design; B - Collection and/or assembly of data; C - Data analysis and interpretation; D - Writing the article; E - Critical revision of the article; F - Final approval of article;
Submission date: 2024-12-07
Final revision date: 2025-04-10
Acceptance date: 2025-04-30
Online publication date: 2025-12-19
Publication date: 2025-12-19
Corresponding author
Richard J. Salvi
Dept. Communication Disorders and Sciences, University of Central Florida, 3280 Progress Drive Ste 500, 32826-3246, Orlando, United States
Dept. Communication Disorders and Sciences, University of Central Florida, 3280 Progress Drive Ste 500, 32826-3246, Orlando, United States
J Hear Sci 2025;1(SPECIAL ISSUE ON MISOPHONIA AND HYPERACUSIS 1):17-32
KEYWORDS
corticosteroneanimal modelsautism spectrum disorderhyperacusisenhanced central gainFragile X syndrome
TOPICS
ABSTRACT
Hyperacusis is a loudness intolerance disorder associated with many medical conditions. To investigate the biological bases of hyperacusis
in animals, we developed an auditory reaction time-intensity (RT-I) paradigm to assess the growth of loudness in rats treated with sodium
salicylate, a drug suspected to cause hyperacusis. Loudness growth was unaffected by low-dose salicylate; however, high doses significantly
reduced reaction times at high intensities, resulting in behavioral evidence of hyperacusis. To identify the neural correlates of salicylate-induced
hyperacusis, neural activity was monitored along the auditory pathway. Salicylate significantly reduced the neural output of the cochlea.
Paradoxically, neural responses were progressively amplified when relayed towards the central auditory pathway resulting in responses 2x larger than normal in auditory cortex (ACx), evidence of enhanced central gain. Because salicylate dose-dependently increased corticosterone stress hormone levels, rats were chronically fed corticosterone stress hormone to determine its behavioral and electrophysiological effects. This led to enhanced sound-evoked neural response in ACx without altering the neural responses from the cochlea and auditory brainstem. Patients with autism often suffer from sound tolerance issues (i.e., hyperacusis). Fragile X (FX) syndrome is a leading genetic cause of autism. To determine if rats with the FX mutation suffered from hyperacusis, we compared loudness growth functions in FX rats with littermate controls. FX rats had normal hearing thresholds but exhibited behavioral evidence of loudness hyperacusis and abnormal temporal and spectral integration of loudness. These behavioral models of hyperacusis can guide the search for biological bases of hyperacusis.
FUNDING
This research and article did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
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