Sönke Ahlf, Konstantin Tziridis, Sabine Korn, Ilona Strohmeyer, Holger Schulze

Dysfunction of the inner ear as caused by presbyacusis, injuries or noise traumata may result in subjective tinnitus, but not everyone suffering from one of these diseases develops a tinnitus percept and vice versa. The reasons for these individual differences are still unclear and may explain why different treatments of the disease are beneficial for some patients but not for others. Here we for the first time compare behavioral and neurophysiological data from hearing impaired Mongolian gerbils with (T) and without (NT) a tinnitus percept that may elucidate why some specimen do develop subjective tinnitus after noise trauma while others do not. Although noise trauma induced a similar permanent hearing loss in all animals, tinnitus did develop only in about three quarters of these animals. NT animals showed higher overall cortical and auditory brainstem activity before noise trauma compared to T animals; that is, animals with low overall neuronal activity in the auditory system seem to be prone to develop tinnitus after noise trauma. Furthermore, T animals showed increased activity of cortical neurons representing the tinnitus frequencies after acoustic trauma, whereas NT animals exhibited an activity decrease at moderate sound intensities by that time. Spontaneous activity was generally increased in T but decreased in NT animals. Plastic changes of tonotopic organization were transient, only seen in T animals and vanished by the time the tinnitus percept became chronic. We propose a model for tinnitus prevention that points to a global inhibitory mechanism in auditory cortex that may prevent tinnitus genesis in animals with high overall activity in the auditory system, whereas this mechanism seems not potent enough for tinnitus prevention in animals with low overall activity.