title: Molecular neurobiological approach to the pathogenesis of epilepsy: a preliminary study.
abstract: We studied the effects and the interactions of some candidate genes related to the pathogenesis of epilepsy using a domestic audiogenic epilepsy-prone rat, matched with the epilepsy-resistant Wistar rat, and primary fetal cerebral cortical neuronal cell cultures of both. The preliminary results showed that there was a possible abnormality of the CCK gene at the post-translational stage in the early postnatal period in P77PMC rat brain; the later rapidly increased rate of CCK-8 synthesis in the hippocampus and subcortical region may represent a compensatory response to the neuronal pathways involved in audiogenic seizures. CCK-8 can decrease the NMDA (1 microM)-induced free intracellular Ca2+ concentration, so it seems to be an inhibitory neuromodulator. In neuronal cell cultures, the NMDA (0.1 microM)-induced c-fos mRNA expression on culture day 18 in vitro was higher in P77PMC than Wistar rats (P < 0.05). Interleukin-1 (20 nM) can induce endogenous opioid mRNA expression and peptide release in neuronal cell cultures, which can be abolished by the addition of antisense oligos of c-fos/c-jun to cell cultures treated with interleukin-1. Both interleukin-1 and opioids can increase the free intracellular Ca2+ concentration, and their specific antagonists can reverse their effects, so they both seem to be excitatory neuromodulators in the CNS.
authors.affiliation: Department of Pediatrics, Beijing Medical University, China.
authors.forename: W
authors.initials: W
authors.lastname: Xi-Ru
authors.forename: W
authors.initials: W
authors.lastname: Zhao-Hui
authors.forename: S
authors.initials: S
authors.lastname: Wai-Song
authors.forename: L
authors.initials: L
authors.lastname: Wei-Lan
authors.forename: Y
authors.initials: Y
authors.lastname: Bao-Qiang
authors.forename: P
authors.initials: P
authors.lastname: Hong
authors.forename: Z
authors.initials: Z
authors.lastname: John-Bao
mesh_terms: D000818:Animals; D002766:Cholecystokinin / Q000032:analysis; D004195:Disease Models, Animal; D004827:Epilepsy / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D017781:Genes, Immediate-Early / Q000502:physiology; D009154:Mutation / Q000502:physiology; D009474:Neurons / Q000737:chemistry / Q000502:physiology; D010865:Pilot Projects; D051381:Rats; D011922:Rats, Mutant Strains; D017208:Rats, Wistar
chemical_list: D002766:Cholecystokinin