Abstract
Tinnitus is the perception of a sound, a so-called “phantom sound,” in the absence of a physical sound. The phantom perception persists after transection of the auditory nerve, indicating that the site of tinnitus manifestation is in the central nervous system. Imaging studies in tinnitus sufferers have revealed increased neuronal activity—hyperactivity—in subcortical and cortical auditory centers. These studies have demonstrated that non-auditory brain areas, such as the limbic system, are involved in the neural basis of tinnitus, Finally human imaging studies have led to novel hypotheses for the generation of tinnitus, such as the thalamocortical dysrhythmia hypothesis. Imaging in animal models of tinnitus exhibit similarities to results from human studies and have revealed hyperexcitability of auditory brain centers as a neural correlate of tinnitus. We propose that the comparison between animal model and human studies will aid in the design of appropriate experimental paradigms aimed at elucidating the cellular and circuit mechanisms underlying tinnitus.
Highlights
Tinnitus sufferers perceive sounds in the absence of any physical auditory stimulus
On the other hand, imaging studies in animal models of tinnitus offer a reduced, better-controlled experimental environment that will facilitate the discovery of the underlying physiological remodeling that leads to tinnitus
The impairment of GABAergic inhibition provides a mechanism for the neural basis of tinnitus-related hyperexcitability in the dorsal cochlear nucleus (DCN) in addition to the known role of impaired glycinergic inhibition after cochlear injury (Suneja et al, 1998a,b; Wang et al, 2009), Together, these studies demonstrate the applicability of imaging techniques—that are analogous to human imaging studies—to study the underlying mechanisms of tinnitus neural correlates
Summary
Imaging the neural correlates of tinnitus: a comparison between animal models and human studies. Imaging studies in tinnitus sufferers have revealed increased neuronal activity—hyperactivity—in subcortical and cortical auditory centers. These studies have demonstrated that non-auditory brain areas, such as the limbic system, are involved in the neural basis of tinnitus, human imaging studies have led to novel hypotheses for the generation of tinnitus, such as the thalamocortical dysrhythmia hypothesis. Imaging in animal models of tinnitus exhibit similarities to results from human studies and have revealed hyperexcitability of auditory brain centers as a neural correlate of tinnitus. We propose that the comparison between animal model and human studies will aid in the design of appropriate experimental paradigms aimed at elucidating the cellular and circuit mechanisms underlying tinnitus
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