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A study of the correlation between myoclonic seizure and molecular mechanism induced by focal cortical dysplasia.

Research Project

Project/Area Number 26461312
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurology
Research InstitutionKyushu University

Principal Investigator

Takase Kei-ichiro  九州大学, 医学研究院, 共同研究員 (00467903)

Co-Investigator(Kenkyū-buntansha) 重藤 寛史  九州大学, 医学研究院, 共同研究員 (50335965)
鎌田 崇嗣  久留米大学, 医学部, 助教 (70614460)
Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Keywordsてんかん / 実験てんかん / ミオクロニー発作 / 皮質異形成 / 動物モデル / 皮質異形性
Outline of Final Research Achievements

On embryonic day (E) 18, a frozen prove was placed on the frontal scalp of a Sprague-Dawley rat embryo through the uterus wall to produce multiple (one or two) freeze lesions on each hemisphere. FCD rat models were divided to group A (one lesion on the left), group B (two lesions on the left) and group C (one lesion on the each frontal areas). All rats were performed EEG monitoring with electrical stimulation onto the scalp electrodes from postnatalday (P) 1 to P7. The number of animals of group C showing myoclonic seizure was significantly more than the other groups on P1, however there was no significance between all groups through the stimulations. Immunoreactivities for N-methyl-D-aspertate receptors and glutamate transporters in FCD lesions were significantly enhanced compared to controls.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report

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Published: 2014-04-04   Modified: 2018-03-22  

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