Abstracts

Rationale: Status epilepticus(SE) during febrile seizure has been known as one of the cause for development of epilepsy. The inflammatory cytokine, interleukin-1β (IL-1β) has been reported to have a neuroinvasive influence on the hippocampus after brain damage including experimental model of SE. We evaluated the expression of IL-1β during the time course of the epileptogenesis using rats with kainic acid-induced status epilepticus. Methods: SE was induced on adult(8-week-old) rats by intraperitoneally administration of kainic acid(10mg/kg). Saline was injected for the controls rats. Two hours after SE, diazepam(10mg/kg) was injected to abort SE. At 12hours and days 1, 3,7,14 and 21 after SE, left brains specimens were fixed in 4% paraformaldehyde and sliced on coronal sections. The expressions of IL-1β on the hippocampus were immunohistochemically examined before and after SE. We homogenized the right hippocampus in RIPA buffer and centrifuged. We measured IL-1β levels of the supernatant using Luminex technology. Results: Spontaneous generalized tonic-clonic seizures appeared on day 7 after SE. Pyramidal cell loss were seen at CA1 and CA3 on day 7. Reactive astrocytes increased with subsequent hypertrophy from day 7 and followed by gliosis. Expressions of IL-1β transiently increased on the pyramidal cells at CA3 on day 1 and then decreased. IL-1β expressed on the reactive astrocytes forming gliosis at CA1 on day 7. The total level of IL-1β in the hippocampus was significantly elevated and maintained after SE. Conclusions: The IL-1β in the hippocampus after SE demonstrated the different expression between the pyramidal cells and the reactive astrocytes in the time course of spontaneous seizures. IL-1β on the reactive astrocytes may contribute to epileptogenesis in the rat with spontaneous seizures post SE and gliotic hippocampus.