Abstract

Induction of hyperactivity in the central auditory system is one of the major physiological hallmarks of animal models of noise-induced tinnitus. Although hyperactivity occurs at various levels of the auditory system, it is not clear to what extent hyperactivity originating in one nucleus contributes to hyperactivity at higher levels of the auditory system. In this study we compared the time courses and tonotopic distribution patterns of hyperactivity in the dorsal cochlear nucleus (DCN) and inferior colliculus (IC). A model of acquisition of hyperactivity in the IC by passive relay from the DCN would predict that the two nuclei show similar time courses and tonotopic profiles of hyperactivity. A model of acquisition of hyperactivity in the IC by compensatory plasticity mechanisms would predict that the IC and DCN would show differences in these features, since each adjusts to changes of spontaneous activity of opposite polarity. To test the role of these two mechanisms, animals were exposed to an intense hyperactivity-inducing tone (10 kHz, 115 dB SPL, 4 h) then studied electrophysiologically at three different post-exposure recovery times (from 1 to 6 weeks after exposure). For each time frame, multiunit spontaneous activity was mapped as a function of location along the tonotopic gradient in the DCN and IC. Comparison of activity profiles from the two nuclei showed a similar progression toward increased activity over time and culminated in the development of a central peak of hyperactivity at a similar tonotopic location. These similarities suggest that the shape of the activity profile is determined primarily by passive relay from the cochlear nucleus. However, the absolute levels of activity were generally much lower in the IC than in the DCN, suggesting that the magnitude of hyperactivity is greatly attenuated by inhibition.

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