Chapter

The salicylate model of tinnitus

Jos J. Eggermont

in The Neuroscience of Tinnitus

Published in print May 2012 | ISBN: 9780199605606
Published online September 2012 | e-ISBN: 9780191741555 | DOI: http://dx.doi.org/10.1093/acprof:oso/9780199605606.003.0006
The salicylate model of tinnitus

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Salicylate induced tinnitus, either following a single high dose or following repeated administration of low dose. Salicylate interacts with the auditory system both in the cochlea and in the central auditory system. In the cochlea it down-regulates the action of prestin in the wall of the outer hair cells and thereby causes a temporary hearing loss. In addition salicylate interacts with the arachidonic acid cycle causing an increase in NMDA receptor activity and increased spontaneous firing rates in auditory nerve fibers. Centrally, salicylate down-regulates serotonin and GABA activity. This makes searching for neural substrates of tinnitus difficult at the least. Salicylate also increases the gain of the more central parts of the auditory system for sound, reflected in increased startle responses and potentially inducing hyperacusis. High levels of salicylate presents variable tend to decrease spontaneous firing rates in primary auditory cortex.

Keywords: arachidonic acid; prestin; hyperacusis; immediate early genes; neurotransmitters; neuromodulators; spontaneous activity; oto-acoustic emissions

Chapter.  10489 words.  Illustrated.

Subjects: Neuroscience

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