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Human Auditory Cortex Neurochemistry Reflects the Presence and Severity of Tinnitus
Journal article   Open access   Peer reviewed

Human Auditory Cortex Neurochemistry Reflects the Presence and Severity of Tinnitus

William Sedley, Jehill Parikh, Richard A. E. Edden, Valerie Tait, Andrew Blamire and Timothy D. Griffiths
The Journal of neuroscience, Vol.35(44), pp.14822-14828
11/04/2015
DOI: 10.1523/JNEUROSCI.2695-15.2015
PMCID: PMC4635131
PMID: 26538652
url
https://doi.org/10.1523/JNEUROSCI.2695-15.2015View
Published (Version of record) Open Access

Abstract

It is not known why tinnitus occurs in some cases of hearing damage but not others. Abnormalities of excitation-inhibition balance could influence whether tinnitus develops and its severity if it does. Animal models of hearing damage, which also produce tinnitus based on behavioral evidence, have identified abnormalities of GABAergic inhibition, both cortically and subcortically. However, the precise relationships of GABA inhibitory changes to tinnitus itself, as opposed to other consequences of hearing damage, remain uncertain. Here, we used magnetic resonance spectroscopy to non-invasively quantify GABA in the left (LAC) and right (RAC) auditory cortices of a group of 14 patients with lateralized tinnitus (eight left ear) and 14 controls matched for age, sex, and hearing. We also explored the potential relationships with other brain metabolites (i.e., choline, N-acetylaspartate, and creatine). The presence of tinnitus was associated with a reduction in auditory cortex GABA concentration. Regardless of tinnitus laterality, post hoc testing indicated reductions that were significant in RAC and nonsignificant in LAC. Tinnitus severity and hearing loss were correlated positively with RAC choline but not GABA. We discuss the results in the context of current models of tinnitus and methodological constraints.
Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Science & Technology

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