Suppression of spontaneous activity in a computational tinnitus DCN model depends on notched-stimulation bandwidth

Abstract

Early tinnitus onset is most likely attributed to an increased spontaneous activity caused by homeostatic plasticity effects in the peripheral auditory system. In a recent modeling study we demonstrated the effects of lateral inhibition on firing regularity related to an increased spontaneous activity. We found that increased activity causes the interconnected neurons to fire more regularly and synchronized. We hypothesized that a suppression of this orchestrated neural activity could be the physiological background of the tailor-made notched acoustic stimulation treatment as proposed by Okamoto and Pantev. In this article we want to highlight this neural activity alignment in the early stages of acoustic processing and examine the effects of different bandwiths of hearing loss and notched stimulation on the increased firing rate. We utilized a computation model of the dorsal cochlear nucleus by Zheng and Voigt with a modified input representing a hearing deficit and tinnitus as well as a notched acoustic stimulation. In-silico results show that the suppression of firing regularity in the frequencyrange of the simulated tinnitus strongly depends on the relationship of the two bandwidths of the hearing deficit and the notched acoustic stimulation. The modulation of neural firing behaviour is thus strongly affected by edge effects, such as lateral inhibition bandwith or the slope of diminished neural excitation due to hearing deficit or stimulus notching.