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This Article Full Text Full Text (PDF) All Versions of this Article: 101/6/3042    most recent 91256.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Schaette, R. Articles by Kempter, R. PubMed PubMed Citation Articles by Schaette, R. Articles by Kempter, R.

Predicting Tinnitus Pitch From Patients' Audiograms With a Computational Model for the Development of Neuronal Hyperactivity

¹Institute for Theoretical Biology, Department of Biology, Humboldt-Universität zu Berlin, Berlin; ²Bernstein Center for Computational Neuroscience Berlin, Berlin; ³Neuroscience Research Center, Charité, Medical Faculty of Berlin, Berlin; and ⁴NeuroCure Center for Neurosciences, Berlin, Germany

Submitted 25 November 2008; accepted in final form 31 March 2009

Tinnitus is often related to hearing loss, but how hearing loss could lead to tinnitus has remained unclear. Animal studies show that the occurrence of tinnitus is correlated to increased spontaneous firing rates of central auditory neurons, but mechanisms that give rise to such hyperactivity have not been identified yet. Here we present a computational model that reproduces tinnitus-related hyperactivity and predicts tinnitus pitch from the audiograms of tinnitus patients with noise-induced hearing loss and tone-like tinnitus. Our key assumption is that the mean firing rates of central auditory neurons are controlled by homeostatic plasticity. Decreased auditory nerve activity after hearing loss is counteracted through an increase of the neuronal response gain, which restores the mean rate but can also lead to hyperactivity. Hyperactivity patterns calculated from patients' audiograms exhibit distinct peaks at frequencies close to the perceived tinnitus pitch, corroborating hyperactivity through homeostatic plasticity as a mechanism for the development of tinnitus after hearing loss. The model suggests that such hyperactivity, and thus also tinnitus caused by cochlear damage, could be alleviated through additional stimulation.