Noise trauma induced behavioral gap detection deficits correlate with reorganization of excitatory and inhibitory local circuits in the inferior colliculus and are prevented by acoustic enrichment.

Noise trauma induced behavioral gap detection deficits correlate with reorganization of excitatory and inhibitory local circuits in the inferior colliculus and are prevented by acoustic enrichment.

J Neurosci. 2017 Jun 05;:

Authors: Sturm JJ, Zhang-Hooks YX, Roos H, Nguyen T, Kandler K

Abstract
Hearing loss leads to a host of cellular and synaptic changes in auditory brain areas, which are thought to give rise to auditory perception deficits such as temporal processing impairments, hyperacusis, or 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 showed a shift in the balance of synaptic excitation and inhibition that was present in both glutamatergic and GABAergic neurons, whereas mice without gap detection deficits showed stable excitation-inhibition balances. Acoustic enrichment with moderate intensity, pulsed white noise immediately following noise trauma prevented both circuit reorganization and gap detection deficits raising the possibility of using acoustic enrichment immediately after cochlear damage to prevent or alleviate the emergence central auditory processing deficits.SIGNIFICANCE STATEMENTNoise overexposure is a major cause of central auditory processing disorders including tinnitus, yet the changes in synaptic connectivity underlying these disorders remain poorly understood. Here we find that brief noise overexposure leads to distinct reorganizations of excitatory and inhibitory synaptic inputs onto glutamatergic and GABAergic neurons, and that the nature of these reorganizations correlates with animals' impairments in detecting brief sound gaps, which is often considered a sign of tinnitus. Acoustic enrichment immediately following noise trauma prevents circuit reorganizations as well as gap detection deficits, highlighting the potential for using sound therapy soon after cochlear damage to prevent the development of central processing deficits.

PMID: 28583912 [PubMed - as supplied by publisher]

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