A COMPUTATIONAL MODEL FOR THE DEVELOPMENT OF TINNITUS-RELATED HYPERACTIVITY

[Emiliano]

A COMPUTATIONAL MODEL FOR THE DEVELOPMENT OF TINNITUS-RELATED HYPERACTIVITY: REDUCTION OF HYPERACTIVITY THROUGH ADDITIONAL ACOUSTIC STIMULATION

Roland Schaette and Richard Kempter

Institute for Theoretical Biology, Humboldt-Universität zu Berlin
Hearing loss through cochlear damage can lead to the development of increased spontaneous firing rates in central auditory neurons. This hyperactivity has been interpreted as a neurophysiological correlate of tinnitus. The earliest stage in the auditory pathway where tinnitus-related changes have been observed is the dorsal cochlear nucleus (DCN), which receives feedforward input from the auditory nerve (AN).

To address the question of how peripheral hearing loss may lead to tinnitus-related hyperactivity of neurons in the auditory brainstem, we utilize a phenomenological model of the responses of AN fibers and DCN neurons. Noise-induced hearing loss reduces the mean activity of the model AN fibers and DCN neurons. We assume that a persistent reduction of the mean firing rate of DCN neurons activates homeostatic
plasticity, a plasticity mechanism that stabilizes neuronal activity on time
scales of hours to days by scaling synaptic strengths and adjusting intrinsic neuronal excitability.

When homeostasis increases the response gain of DCN neurons after hearing loss, the mean firing rate can be restored to its pre-lesion values, but the spontaneous firing rate may be increased above the normal level. Thus, in our model, hyperactivity is a consequence of a central compensation for decreased AN activity, implying that hyperactivity could be decreased through additional acoustic stimulation. When additional acoustic stimulation increases the activity of model AN fibers and
DCN neurons, the pathologically increased response gain of DCN neurons is lowered, and hyperactivity is reduced. The duration of hyperactivity suppression in the model depends on the time-scale of the gain adaptation. As homeostatic plasticity is a slow process, a long-lasting reduction of hyperactivity after stimulation could be possible.