Journal
JOURNAL OF NEUROSCIENCE
Volume 37, Issue 26, Pages 6314-6330Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0602-17.2017
Keywords
midbrain; noise trauma; tinnitus; uncaging
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Funding
- National Institutes of Health (National Institute on Deafness and Communication Disorders Grant) [04399, 1F30DC014177]
- University of Pittsburgh Physicians Academic Foundation
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Hearing loss leads to a host of cellular and synaptic changes in auditory brain areas that are thought to give rise to auditory perception deficits such as temporal processing impairments, hyperacusis, and tinnitus. However, little is known about possible changes in synaptic circuit connectivity that may underlie these hearing deficits. Here, we show that mild hearing loss as a result of brief noise exposure leads to a pronounced reorganization of local excitatory and inhibitory circuits in the mouse inferior colliculus. The exact nature of these reorganizations correlated with the presence or absence of the animals' impairments in detecting brief sound gaps, a commonly used behavioral sign for tinnitus in animal models. Mice with gap detection deficits (GDDs) showed a shift in the balance of synaptic excitation and inhibition that was present in both glutamatergic and GABAergic neurons, whereas mice without GDDs showed stable excitationinhibition balances. Acoustic enrichment (AE) with moderate intensity, pulsed white noise immediately after noise trauma prevented both circuit reorganization and GDDs, raising the possibility of using AE immediately after cochlear damage to prevent or alleviate the emergence of central auditory processing deficits.
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