Tinnitus: pathology of synaptic plasticity at the cellular and system levels

Guitton, Matthieu J.

doi:10.3389/fnsys.2012.00012

Cited by 40 publications

(39 citation statements)

References 52 publications

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“…In summary, it is now clear that tinnitus is a pathology involving synaptic plasticity (Guitton, 2012). The origin of tinnitus can occur either at the level of the synapses between inner hair cells and the auditory nerve, within the auditory nerve itself, or from CAS structures.…”

Section: Discussionmentioning

confidence: 99%

Underlying Mechanisms of Tinnitus: Review and Clinical Implications

et al. 2014

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Background The study of tinnitus mechanisms has increased tenfold in the last decade. The common denominator for all of these studies is the goal of elucidating the underlying neural mechanisms of tinnitus with the ultimate purpose of finding a cure. While these basic science findings may not be immediately applicable to the clinician who works directly with patients to assist them in managing their reactions to tinnitus, a clear understanding of these findings is needed to develop the most effective procedures for alleviating tinnitus. Purpose The goal of this review is to provide audiologists and other health-care professionals with a basic understanding of the neurophysiological changes in the auditory system likely to be responsible for tinnitus. Results It is increasingly clear that tinnitus is a pathology involving neuroplastic changes in central auditory structures that take place when the brain is deprived of its normal input by pathology in the cochlea. Cochlear pathology is not always expressed in the audiogram but may be detected by more sensitive measures. Neural changes can occur at the level of synapses between inner hair cells and the auditory nerve and within multiple levels of the central auditory pathway. Long-term maintenance of tinnitus is likely a function of a complex network of structures involving central auditory and nonauditory systems. Conclusions Patients often have expectations that a treatment exists to cure their tinnitus. They should be made aware that research is increasing to discover such a cure and that their reactions to tinnitus can be mitigated through the use of evidence-based behavioral interventions.

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Section: Discussionmentioning

confidence: 99%

Underlying Mechanisms of Tinnitus: Review and Clinical Implications

et al. 2014

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“…Its origin may be ongoing abnormal neural brain activity, neural plasticity, disturbed brain network, damage of hair cells in the inner ear, sudden-onset hearing loss, head trauma, among other sources (Bauer et al, 2013;Guitton, 2006Guitton, , 2012Maudoux et al, 2012a;Vanneste and De Ridder, 2012;Zheng et al, 2011). In contrast, PT is considered to be an auditory percept by the stimulation of hair cells in the inner ear (Levine et al, 2008;Madani and Connor, 2009;Sonmez et al, 2007;Waldvogel et al, 1998).…”

Section: Introductionmentioning

confidence: 89%

Disrupted neural activity in unilateral vascular pulsatile tinnitus patients in the early stage of disease: Evidence from resting-state fMRI

Liu

Yan

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…The chemical induction of tinnitus through the action of salicylate (active compound of aspirin) is alleviated when NMDARs are blocked (Guitton et al, 2003), indicating that salicylate induces tinnitus through its ability to modulate NMDA-R function. A proposed mechanism suggests salicylate causes overactivation of NMDA-Rs and susceptibility of SGNs to aberrant excitation, generating symptoms associated with tinnitus (Guitton, 2012).…”

Section: Mammalian Inner Hair Cell-spiral Ganglion Neuron (Ihc-sgn) Smentioning

confidence: 99%

From development to disease: Diverse functions of NMDA-type glutamate receptors in the lower auditory pathway

Sanchez

Ghelani²,

Otto-Meyer³

2015

Neuroscience

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N-methyl-D-aspartate receptors (NMDA-Rs) are located at each synapse in the lower auditory pathway of mammals and avians. Characterized by a slow and long-lasting excitatory response upon glutamate activation, their existence in a sensory system biologically engineered for speed and precision seems counterintuitive. In this review we consider the diverse functions of NMDA-Rs. Their developmental regulation and unique subunit composition in the inner ear promote protective and neurotrophic roles following acute insult by regulating AMPA-R expression and assisting in the restoration of synaptic inputs. This contrasts with chronic damage where overactivation of NMDA-Rs is implicated in neuronal death. These functions are thought to be involved in auditory diseases, including noise-induced hearing loss, neural presbycusis, and tinnitus via aberrant excitation. A more traditional role emerges in the developing auditory brainstem, where NMDA-Rs are downregulated and switch subunit composition with maturation. Their biophysical properties also contribute to synaptic dynamics resembling long-term plasticity. At mature synapses they support reliable auditory processing by increasing the probability of action potential generation, regulating first-spike latency, and maintaining reliable action potential firing. Thus, NMDA-R functions in the lower auditory pathway are diverse, contributing to synaptic development, plasticity, temporal processing, and diseases.

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Tinnitus: pathology of synaptic plasticity at the cellular and system levels

Cited by 40 publications

References 52 publications

Underlying Mechanisms of Tinnitus: Review and Clinical Implications

Underlying Mechanisms of Tinnitus: Review and Clinical Implications

Disrupted neural activity in unilateral vascular pulsatile tinnitus patients in the early stage of disease: Evidence from resting-state fMRI

From development to disease: Diverse functions of NMDA-type glutamate receptors in the lower auditory pathway

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