Abstract
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.
Highlights
Diseases of the inner ear leading to hearing loss (HL) may result in subjective tinnitus [1]
The example of an animal with a spectrally narrow tinnitus percept shown in the left panel of Figure 2A had a significant prepulse inhibition (PPI) impairment at 4 and 8 kHz only (Tukey post-hoc tests after one-factorial ANOVA)
To achieve this goal we employed a multistep procedure: First, we quantified the noise trauma induced hearing loss using both electrophysiological (ABR) and behavioral approaches (PPI of auditory startle response (ASR)) which led to similar estimates of hearing loss
Summary
Diseases of the inner ear leading to hearing loss (HL) may result in subjective tinnitus [1]. In this report we follow the hypothesis that there must be some predisposition in the central auditory system of some but not all individuals that protects them from the development of subjective tinnitus In search of this predisposition we recorded neuronal activity from the auditory brainstem and cortex of the same individuals of Mongolian gerbils before and after an acoustic trauma and compared the data obtained from animals that showed an acute tinnitus percept in behavioral testing (group T) with data from those that did not (group NT). Possible differences in these two groups of animals may further elucidate the neuronal mechanisms that lead to subjective tinnitus and thereby may help to find a prophylaxis against tinnitus development and improve actual treatments for tinnitus patients (e.g. [10])
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