Modeling the cellular and circuit mechanisms underlying the neural correlates of tinnitus.
Tinnitus, a disease characterized by the persistent perception of a subjective sound, is accompanied by increased firing rates and hyper-synchronous activity in many auditory areas. The mechanisms that underly tinnitus-related changes in neural activity are ill understood. In a mouse model of tinnitus, the principal cells of the dorsal cochlear nucleus (DCN) have significantly weaker after- hyperpolarization (AHP) currents. They recover much more quickly after firing an action potential, so a reduction in AHP current will lead to increased firing rates. It remains, however, to consider how AHP currents affects the synchronization of pairs of neurons’ activity. Using a combination of simulations and mathematical theory we show that weakened AHP currents, consistent with those of DCN principal cells of tinnitus mice, increase both the firing rate and covariability of spike train responses. Furthermore, we show that the increase in covariability is not just due to the increase in firing rate. We show that these results are not obvious from past theories linking firing rate and covariability and uncover a novel relationship between single-neuron biophysics and pairwise spiking statistics, linking intrinsic negative feedback and pairwise covariable activity.