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      Central Gain Control in Tinnitus and Hyperacusis

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          Sensorineural hearing loss induced by noise or ototoxic drug exposure reduces the neural activity transmitted from the cochlea to the central auditory system. Despite a reduced cochlear output, neural activity from more central auditory structures is paradoxically enhanced at suprathreshold intensities. This compensatory increase in the central auditory activity in response to the loss of sensory input is referred to as central gain enhancement. Enhanced central gain is hypothesized to be a potential mechanism that gives rise to hyperacusis and tinnitus, two debilitating auditory perceptual disorders that afflict millions of individuals. This review will examine the evidence for gain enhancement in the central auditory system in response to cochlear damage. Further, it will address the potential cellular and molecular mechanisms underlying this enhancement and discuss the contribution of central gain enhancement to tinnitus and hyperacusis. Current evidence suggests that multiple mechanisms with distinct temporal and spectral profiles are likely to contribute to central gain enhancement. Dissecting the contributions of these different mechanisms at different levels of the central auditory system is essential for elucidating the role of central gain enhancement in tinnitus and hyperacusis and, most importantly, the development of novel treatments for these disorders.

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              Homeostatic synaptic scaling is a form of synaptic plasticity that adjusts the strength of all of a neuron's excitatory synapses up or down to stabilize firing. Current evidence suggests that neurons detect changes in their own firing rates through a set of calcium-dependent sensors that then regulate receptor trafficking to increase or decrease the accumulation of glutamate receptors at synaptic sites. Additional mechanisms may allow local or network-wide changes in activity to be sensed through parallel pathways, generating a nested set of homeostatic mechanisms that operate over different temporal and spatial scales.

                Author and article information

                URI :
                URI :
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                Front Neurol
                Front Neurol
                Front. Neurol.
                Frontiers in Neurology
                Frontiers Media S.A.
                24 October 2014
                : 5
                1Department of Communicative Disorders and Sciences, Center for Hearing and Deafness, University at Buffalo, The State University of New York , Buffalo, NY, USA
                Author notes

                Edited by: Jinsheng Zhang, Wayne State University, USA

                Reviewed by: Aasef G. Shaikh, Case Western Reserve University, USA; Bin Liu, Wayne State University, USA; Edward Pace, Wayne State University, USA

                *Correspondence: Richard J. Salvi, Department of Communicative Disorders and Sciences, Center for Hearing and Deafness, University at Buffalo, The State University of New York, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, USA e-mail: salvi@

                Benjamin D. Auerbach and Paulo V. Rodrigues have contributed equally to this work.

                This article was submitted to Neuro-otology, a section of the journal Frontiers in Neurology.

                Copyright © 2014 Auerbach, Rodrigues and Salvi.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Figures: 8, Tables: 0, Equations: 0, References: 285, Pages: 21, Words: 19859
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                homeostatic plasticity, lateral inhibition, central gain enhancement, hyperacusis, tinnitus


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