Hearing loss from intense noise exposure and ototoxic drugs greatly reduces the neural output of the cochlea. Despite a reduced cochlear output, neural activity in the central auditory pathway often becomes hyperactive at suprathreshold intensities indicative of Enhanced Central Gain. Enhanced Central Gain is believed to be responsible for hyperacusis, a condition in which listeners experience everyday sounds as unbearably loud or even painful. The goals of this project are: (1) Determine if Enhanced Central Gain is responsible for the temporal and spectral features of hyperacusis, (2) Determine how the acoustic environment (sound enrichment/deprivation) modulates hyperacusis/loudness growth and Central Gain and (3) Determine how serotonin and GABA agonists/antagonists affect hyperacusis and Central Gain. The proposed studies will increase our understanding of the neural mechanisms of hyperacusis and test the efficacy of pharmacological agents to treat hyperacusis.

Public Health Relevance

Individuals with cochlear hearing loss suffer from hyperacusis (loudness intolerance), a condition thought to arise from increased neural gain in the central auditory pathway. A series of experiments is planned to: (1) determine if the time course and spectral features of increased Central Gain matches the time course and spectral properties of hyperacusis (2) determine how acoustic stimulation/deprivation affects hyperacusis, loudness growth and Central Gain and (3) assess the effects of serotonergic and GABAergic drugs on hyperacusis and Central Gain. The proposed studies will provide both clinical and basic science insights relevant to understanding and treating hyperacusis.

National Institute of Health (NIH)
National Institute on Deafness and Other Communication Disorders (NIDCD)
Research Project (R01)
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Special Emphasis Panel (ZRG1-IFCN-B (02)M)
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Miller, Roger
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State University of New York at Buffalo
Other Health Professions
Schools of Arts and Sciences
United States
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