Pathomechanisms underlying human temporal lobe epilepsy

2016 Fiscal Year Final Research Report

• Project/Area Number: 25250008
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Nerve anatomy/Neuropathology
• Research Institution: Niigata University
• Principal Investigator: KAKITA Akiyoshi 新潟大学, 脳研究所, 教授 (80281012)
• Co-Investigator(Kenkyū-buntansha): 藤井 幸彦 新潟大学, 脳研究所, 教授 (40283014) ; 北浦 弘樹 新潟大学, 脳研究所, 助教 (80401769)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: てんかん / 脳神経疾患 / 海馬硬化症 / カリウムチャネル / 海馬

Outline of Final Research Achievements

Mesial temporal lobe epilepsy (MTLE) is the most frequent focal epileptic syndrome in adults, and the majority of seizures originate primarily from the hippocampus. The resected hippocampus shows several degrees of neuronal loss (hippocampal sclerosis: HS), accordingly there would arise a paradox between clinical and pathological findings; how these atrophic tissues cause epilepsy? Here we investigated epileptiform activities using hippocampal specimens taken from MTLE patients ex vivo. Flavoprotein fluorescence imaging and local field potential recordings (LFPs) revealed that epileptiform activities were arise from subiculum of MTLE groups. Moreover, loss of inwardly rectifying K+ channel 4.1 (Kir 4.1) was evident in the astrocytes of the subiculum of HS. These results suggest that epileptogenic mechanisms would correlate to the distinct pathologies, and Kir 4.1 may play a pivotal role in epileptogensis of the HS.

Free Research Field

神経病理学