2012 Fiscal Year Final Research Report
Mechanism and prevention strategy for mesial temporallobe epilepsy following febrile status convulsion
| Project/Area Number |
22591132
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | Ehime University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Yuka 愛媛大学, 大学院・医学系研究科, 寄附講座准教授 (00304634)
EGUCHI Minenari 愛媛大学, 医学部附属病院, 講師 (50420782)
TANAKA Junya 愛媛大学, プロテオ医学研究センター, 教授 (70217040)
|
|---|
| Project Period (FY) |
2010 – 2012
|
| Keywords | 熱性けいれん / 内側側頭葉てんかん / けいれん重積 / サイトカイン / 動物モデル |
|---|
| Research Abstract |
Febrile seizures (FS) are recognized as an antecedent to the development of temporal lobe epilepsy with hippocampal sclerosis (TLE-HS). In this study, we used a rat model of FS to study the effects of inflammatory cytokines on seizure susceptibility and neuronal death in adulthood. Prolonged hyperthermia-induced seizures (pHS) were induced in male Lewis rats on P10 and 12, and IL-1β were administered twice intranasally at the seizures. Adulthood seizure susceptibility (P70) was significantly enhanced in rats receiving IL-1β together with repeated pHS, whereas no significant effects were seen in rats receiving IL-1β after a single pHS episode (P10). Significant hippocampal neuronal cell loss was observed in the CA3 region of rats receiving IL-1β together with repeated pHS. Our results are consistent with the hypothesis that excessive production of IL-1β after repeated prolonged FS could enhance adulthood seizure susceptibility and neuronal cell death, and might contribute tothe development of TLE-HS.
|
