Keynote Lecture

Prof. Dr. Holger Schulze
Experimental Otolaryngology
University of Erlangen-Nuremberg

A model of tinnitus development – from cochlea to cortex

Subjective tinnitus, the perception of sound in the absence of a physical sound source, is a frequent symptom with increasing prevalence, currently affecting 10 to 15% of the adult general population. Because the mechanisms leading to the condition are still not fully understood, a cure for subjective tinnitus is still not available. Common models of tinnitus development propose that damage to the peripheral auditory epithelium in cochlea leads to an imbalance of excitatory and inhibitory auditory circuits, thereby enhancing neuronal activity. Other models propose homeostatic plasticity within the central auditory system attempting to compensate for reduced cochlear input via an increased response gain.

Here we propose an alternative model based on stochastic resonance (SR) which serves to lift signals above noise trauma induced increased neuronal thresholds, thereby partly compensating for the hearing loss. In that view, the internally generated noise - which is crucial for SR to work - corresponds to neuronal hyperactivity which subsequently causes neuronal plasticity along the auditory pathway and finally may lead to the development of a phantom percept, i.e. subjective tinnitus. In addition, we show evidence from our animal model, the Mongolian gerbil, that such tinnitus development is closely associated with synaptopathy at inner hair cells rather than increased hearing thresholds per se. Finally, we demonstrate that when tinnitus manifests, neuronal activation patterns in auditory cortex that are associated with spontaneous activity, i.e. that are recorded during silence, become similar to those evoked by pure tones matching the perceived tinnitus frequency.