Abstract
Emerging evidence suggests that the immune system may signifi cantly contribute to seizures and epilepsy. The kindling and status epilepticus models of epilepsy provide valuable tools with which to study mechanisms underlying epileptogenesis. Epileptogenesis refers to a dynamic process that progressively alters neuronal excitability and causes reorganization of neuronal networks before the fi rst spontaneous seizure occurs. The infl ammatory changes during epileptogenesis include gliosis and activation of microglia, blood–brain barrier damage and an increase in the expression of proinfl ammatory cytokines. Several studies have demonstrated that the activation of proinfl ammatory pathways infl uences neurotransmitter systems and neuronal excitability, thereby contributing to epileptogenesis. The infl ammatory pathways represent a promising new target for the development of new drugs, that can prevent epileptogenesis. Various pharmacologic studies report inhibition of seizures and blocking the epileptogenesis by using nonsteroidal anti-infl ammatory drugs and immunosuppressants.