Circadian control of neural excitability in an animal model of temporal lobe epilepsy.

We provide experimental evidence for the emerging imbalance in the firing activity of two distinct classes (type 1 and type 2) of population spikes recorded from the hippocampal area CA1 in an animal model of temporal lobe epilepsy. We show that during the latent period of epileptogenesis following status epilepticus inducing brain injury, there is a sustained increase in the firing rate of type 1 population spikes (PS1) with a concurrent decrease in the firing rate of type 2 population spikes (PS2). Both PS1 and PS2 firing rates are observed to follow a circadian rhythm and are in-phase in control rats. Following brain injury there is an abrupt phase shift in the circadian activity of the PS firing rates. We hypothesize that this abrupt phase shift is the underlying cause for the emergence of imbalance in the firing activity of the two PS. We test our hypothesis in the framework of a simple two-dimensional Wilson-Cowan model that describes the interaction between firing activities of populations of excitatory and inhibitory neurons.