Abstract
We performed magnetic resonance spectroscopy (MRS) on healthy individuals with tinnitus and no hearing loss (n = 16) vs. a matched control group (n = 17) to further elucidate the role of excitatory and inhibitory neurotransmitters in tinnitus. Two-dimensional J-resolved spectroscopy (2D-JPRESS) was applied to disentangle Glutamate (Glu) from Glutamine and to estimate GABA levels in two bilateral voxels in the primary auditory cortex. Results indicated a lower Glu concentration (large effect) in right auditory cortex and lower GABA concentration (medium effect) in the left auditory cortex of the tinnitus group. Within the tinnitus group, Glu levels positively correlated with tinnitus loudness measures. While the GABA difference between groups is in line with former findings and theories about a dysfunctional auditory inhibition system in tinnitus, the novel finding of reduced Glu levels came as a surprise and is discussed in the context of a putative framework of inhibitory mechanisms related to Glu throughout the auditory pathway. Longitudinal or interventional studies could shed more light on interactions and causality of Glu and GABA in tinnitus neurochemistry.
Highlights
Tinnitus is a condition in which the affected individuals experience a persistent sound in one or both ears, or in the head
In a human magnetic resonance spectroscopy (MRS) study, a GABA deficit in the right auditory cortex was found in individuals suffering from tinnitus compared to healthy individuals[16]
Cases with artifacts caused by remaining lipid peaks or residual water peaks were rejected in order to ensure valid results of the statistical analyses
Summary
Tinnitus is a condition in which the affected individuals experience a persistent sound in one or both ears, or in the head This definition has been expanded to include a differentiation between the auditory phantom perception and a (related) disorder, characterized by high levels of distress[1]. The role of these activity increases in the form of neuronal hyperactivity, bursting discharges and increased cortical neural synchrony in tinnitus pathogenesis is still unresolved but might be a result of lack of inhibition in the central auditory p athway[10,11]. Cochlear damage results in a redistribution of these receptor subtypes in the CN, where an up-regulation of non-auditory Glu receptors (VGLUT2) in the CN could be observed[18] This increased glutamatergic input could be responsible for increased spontaneous firing rates in the CN neurons, which is proposed as a correlate of the tinnitus sensation. While many studies indicate a shift in the balance of excitation/inhibition towards excitation in the auditory system of individuals with tinnitus, a consistent theory of the influences of the various neurotransmitters does not yet exist
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