Self-connection of Thalamic Reticular Nucleus Modulating Absence Seizures

Abstract

Accumulating evidence has suggested that the corticothalamic system not only underlies the onset of absence seizures, but also provides functional roles in controlling absence seizures. However, few studies are involved in the roles of self-connection of thalamic reticular nucleus (TRN) in modulating absence seizures. To this end, we employ a biophysically based corticothalamic network mean-field model to explore these potential control mechanisms. We find that the inhibitory projection from the TRN to specific relay nuclei of thalamus (SRN) can shape the self-connection of TRN controlling absence seizures. Under certain condition, the self-connection of TRN can bidirectionally control absence seizures, which increasing or decreasing the coupling strength of the self-connection of TRN could successfully suppress absence seizures. These findings might provide a new perspective to understand the treatment of absence epilepsy.