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Molecular Mechamis of West Syndrome

Research Project

Project/Area Number 06670831
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Pediatrics
Research InstitutionJikei University, School of Medicine

Principal Investigator

HORITA Hideki  Jikei University, School of Medicine, Department of Pediatrics, Assistant Professor, 医学部, 講師 (50057080)

Co-Investigator(Kenkyū-buntansha) NOZAKI Hidetsugu  Jikei University School of Medicine, Department of Pediatrics, Assistant, 医学部, 助手 (20189393)
MATSUSHIMA Hiroshi  Jikei University School of Medicine, Department of Pediatrics, Assistant Profess, 医学部, 講師 (70190460)
MAEKAWA Kihei  Jikei University School of Medicine, Department of Pediatrics, Professor, 医学部, 教授 (80056613)
Project Period (FY) 1994 – 1995
Project Status Completed (Fiscal Year 1995)
Budget Amount *help
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
KeywordsWest syndrome / Corticotropin releasing hormone / Epilepsy / 遺伝子導入
Research Abstract

We have investigated the molecular mechanisms of West syndrom which is characterized by generalized myoclonic seizure (infantile spasms), hypsarrythmia, and developmental delay. Although ACTH therapy has been used and though to be very effective to the syndrome for long time, the dstailed molecular mechanisms of the disease has not been understood. We hypothesized that increased level of corticotropin releasing hormone (CRH) in the immature brain induces West syndrome. To test this hypothesis, we transfected the CRH cDNA into the undifferentiated neuroblast in vitro and established the transfectants expressing the various level of CRH.The transfectants were induced to either neuronal or glial phenotype depends on the extrinsic factors that were added to the culture medium. However, the level of CRH produced by the transfectants was unaffected, and maintained the constant level of CRH exprerssion. These transfectants are now useful to investigate the roles of CRH on West syndrome. The transfectants will be injectes into the mouse brain and tasted whether the increased level of CRH elicites the epileptic seizure in vivo.

Report

(3 results)
  • 1995 Annual Research Report   Final Research Report Summary
  • 1994 Annual Research Report
  • Research Products

    (7 results)

All Other

All Publications (7 results)

  • [Publications] 堀田秀樹: "強直発作を頻発する例のポリソノグラフィ" 臨床脳波. 37. 132-134 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] H. Matsushima: "Constitutive N-myc gene expression inhibits trkA mediated neuronal differentiation." Oncogene. 10. 1915-1925 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Hideki Horita: "A Study of Atypical Benign Partial Epilepsy of Childhood (ABPE) by Means of Long Term EEG Recording." Epilepsy Research. 12. 23-27 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Hideki Horita: "Clinical Study of Nonepileptic Seizures in Childhood." Child Health Research. 53. 549-552 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Hideki Horita: "Polysomnography of a child with frequent tonic seizures." Clinical EEG. 37. 132-134 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] 堀田秀樹: "強直発作を頻発する例のポリソノグラフィ" 臨床脳波. 37. 132-134 (1995)

    • Related Report
      1995 Annual Research Report
  • [Publications] H. Matsushima: "Constitutive N-myc gene expression inhibits trkA mediated neuronal differentiation." Oncogene. 10. 1915-1925 (1995)

    • Related Report
      1995 Annual Research Report

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Published: 1994-04-01   Modified: 2016-04-21  

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