Regulatory mechanism of inhibitory interneurons with time-delay on epileptic seizures under sinusoidal sensory stimulation.

Abstract

Epilepsy is a neurological disorder in which complex electrophysiological processes are closely linked to inherent nonlinear kinetic properties. This study investigates the effects of sinusoidal sensory stimulation bias and time-delay on the dynamics of epileptic seizures within a corticothalamic neural network model. The results indicate that an increase in sensory stimulation bias can prematurely terminate seizures, and high-frequency stimulation can induce a phenomenon of frequency resonance. Meanwhile, discharge states transitions are associated with the emergence of bifurcation points. Time-delay exerts a significant regulatory influence on pathways with delay embedding (I2-PY), whereas its impact on pathways without delay embedding (I1-I1 and thalamic relay nucleus (TC)-I2) is negligible. Under sinusoidal sensory stimulation, the responses of three pathways (I1-I1, I1-PY, and I2-PY) associated with inhibitory interneurons reveal that the inhibitory properties of interneurons can suppress seizures; however, an excessively strong inhibitory effect may also precipitate seizures and facilitate state transitions. These findings contribute to a deeper understanding of seizure dynamics and may guide future research in the transmission and evolution of seizures.