Chapter 27 Preliminary molecular neurobiology study on the pathogenesis of primary epilepsy

Abstract

Publisher Summary This chapter presents experiments to study the effects and interaction of cholecystokinin (CCK), immediate early genes (IEGs) and N-methyl-D-aspartate (NMDA) receptor on the pathogenesis of epilepsy. The studies used both in vivo and in vitro models. The in vivo model was a domestic audiogenic epilepsy-prone rat P77PMC using epilepsy-resistant rat Wistar as control. The in vitro model involved cortical neuronal cell cultures prepared from fetal cerebral cortex. Studies show that P77PMC rat was not only susceptible to audiogenic seizures, but also to hyperthermic and Kainic acid-induced seizures. This rat seems to be one of the ideal animal models for studying the primary generalized epilepsy-related factors. There are multiple candidate genes that may contribute to the pathogenesis of epilepsy. The pathogenesis of epilepsy may be affected by genetical and/or environmental factors. These abnormal factors interact with each other, which may determine the phenotype of neurons. The change of the neuronal phenotype may induce the changes of seizure susceptibility. Despite the fact that neither NMDA receptor, c-fos, nor CCK genes are located in either chromosome 6p or 20q, their interaction may create the possibility of modifying the pathways leading to epileptic seizures. Some of the candidate genes with suppression effect on seizure may be identified that can then be used for the development of antisense oligos.