Transition dynamics and optogenetic control of epileptiform activity in a modified mean filed model of human cortex

Abstract

Physiological experiments have shown that inhibitory interneurons can induce and maintain epileptiform activities, and different interneuron subtypes may be responsible for different types of seizures. Here we aim to link these electrophysiological experimental phenomena with theoretical dynamic mechanisms based on an improved Liley mean field model. Fascinatingly, the number of synapses between inhibitory neural populations can induce a rich state transition. Typically, the system will experience normal rhythm discharges, multispike discharges, spike wave discharges (SWD), generalized periodic discharges (GPD), the beta band oscillation, and eventually return to the normal state. Interestingly, the transition process can also be reversed. Meanwhile, disinhibition circuits can cause more epileptiform activities after taking into account the delay of synaptic information transmission. Furthermore, we are committed to designing different control strategies for epileptiform activities. As we expected, both deep brain stimulation and optogenetic technology can destroy or even eliminate pathological waves. It is need to emphasis that the cell type specificity of optogenetic regulation allows it to precisely target inhibitory neural populations, which is agree with experiment. Particularly, three different optogenetic regulatory strategies targeting inhibitory neural populations are modeled and proposed, of which the intermittent is designed to save energy. These modeling results reproduce the experimental phenomena and more significantly, help understand the mechanism of epilepsy to guide the clinical practice.