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Cyte-physiological study of abnormal Ca^<2+> metabolism in delayed neuronal death

Research Project

Project/Area Number 15591543
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Cerebral neurosurgery
Research InstitutionJichi Medical School

Principal Investigator

OGURO Keiji  Jichi Medical School, Surgical Neurology, Assistant professor, 医学部, 講師 (90231232)

Co-Investigator(Kenkyū-buntansha) SHIMAZAKI Kuniko  Jichi Medical School, Physiology, Assistant professor, 医学部, 講師 (40142153)
WATANABE Eiju  Jichi Medical School, Surgical Neurology, Professor, 医学部, 教授 (50150272)
Project Period (FY) 2003 – 2004
Project Status Completed (Fiscal Year 2004)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥2,200,000 (Direct Cost: ¥2,200,000)
Keywordscerebral ischemia / calcium / hippocampus / resistance / slice / GluR2 / IP_4
Research Abstract

Ischemic resistance of developing gerbils
To investigate the mechanisms by which developing animals exhibit ischemic resistance, we examined the changes in intracellular calcium ([Ca^<2+>]i) after oxygen-glucose deprivation (OGD) using hippocampal slices form gerbils. We found that increases in [Ca^<2+>]i in hippocampal CA1 neurons is significantly less after OGD in developing gerbils than in adults. We then examined the expression of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid) receptors (AMPARs) GluR1-4 during the developmental period by Western blot analysis. We also investigated the anti-apoptotic proteins HSP70,Bcl-XL and plasma membrane Ca^<2+>-ATPase type 1 (PMCA1). GluR2 expression, but not that of the other AMPARs, is significantly higher in developing gerbils than in adults. These results suggest that the higher expression of GluR2 is important for the smaller increases in [Ca^<2+>]i and enhanced resistance to ischemia-induced neuronal damage in developing anim … More als.
Functional changes in IP_33 kinase knock-out mice
IP_33-kinase metabolizes IP_3 to 1,3,4,5-tetrakisphosphate (IP_4). Until recently physiological roles of IP_33-kinase or IP_4 are not well known. IP_33-kinase (A) is abundant in neuronal cells and IP_4 level in IP_33-kinase(A) deficient mice is significantly decreased. To know the role of IP_33-kinase or IP_4 in neuronal tissue, histochemical, behavioral and physiological study were performed using IP_33-kinase(A) deficient and wild type mice. In histochemical study with IP_33-kinase antibody, IP_33-kinase strongly express in hioppocampal CA1 region in normal gerbil. Passive avoidance with electric shocking chamber revealed less learning and memory function in IP_33-kinase(A) deficient mice. Hippocampal damage induced by global ischemia by 10 min common carotid occlusion did not show significant differences between IP_33-kinase(A) deficient and wild type mice. Intracellular Ca^<2+> increase following oxygen-glucose deprivation was also examined using hippocampal slice of deficient and wild type mice. These results suggest that IP_33-kinase and IP_4 have important roles in the process of learning and memory. Less

Report

(3 results)
  • 2004 Annual Research Report   Final Research Report Summary
  • 2003 Annual Research Report
  • Research Products

    (12 results)

All 2005 2004 2003 Other

All Journal Article (8 results) Book (2 results) Publications (2 results)

  • [Journal Article] Ischemic tolerance with 3-nitropionic acid induces the over expression of Bcl-2 and Bcl-x_L but lacking for HSP70 and plasma membrane Ca_<2+>-ATPase type12005

    • Author(s)
      Kato K, Shimazaki K, Kamiya T, Amemiya S, Inaba T, Oguro K, Katayama Y
    • Journal Title

      Life Sci (in press)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Ischemic tolerance with 3-nitropionic acid induces the over expression of Bcl-2 and Bcl-_<XL> but lacking for HSP70 and plasma membrane Ca^<2+>-ATPase type 1.2005

    • Author(s)
      Kato K, Shimazaki K, Kamiya T, Amemiya S, Inaba T, Oguro K, Katayama Y.
    • Journal Title

      Life Science (in press)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Upregulation of GluR2 decreases intracellular Ca^<2+> following ischemia in developing gerbils2004

    • Author(s)
      Oguro K, Miyawaki T, Yokota H, Kato, M, Watanabe M, Shimazaki K, et al.
    • Journal Title

      Neurosci.Letter 364

      Pages: 101-105

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Ischemic preconditioning decreases intracellular zinc accumulation induced by oxygen-glucose deprivation in gerbil hippocampal CA1 neurons2004

    • Author(s)
      Miyawaki T, Yokota H, Oguro K, Yokota H, Kato K, Shimazaki K.
    • Journal Title

      Neurosci.Letter 362

      Pages: 216-219

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Annual Research Report 2004 Final Research Report Summary
  • [Journal Article] Ischemic preconditioning decreases oxgen-glucose deprivation induced intracellular zink accumulation in gerbil hippocampal CA1 neurons.2004

    • Author(s)
      Miyawaki T, Yokota H, Oguro K, Kato K, Shimazaki K.
    • Journal Title

      Neurosci Letters 362

      Pages: 216-219

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Upregulation of GluR2 decreases intracellular Ca2+ following ischemia in developing gerbils.2004

    • Author(s)
      Oguro K, Miyawaki T, Hokota H, Kato K, Kamiya T, Katayama Y, Fukaya M, Watanabe M, Shimazaki K.
    • Journal Title

      Neurosci Letters 364

      Pages: 101-105

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Upregulation of GluR2 decreases intracellular Ca^<2+> following ischemia in developing gerbils2004

    • Author(s)
      Oguro K, Miyawaki T, Yokota H, Kato M, Watanabe M, Shimazaki K, et al.
    • Journal Title

      Neurosci.Letter 364

      Pages: 101-105

    • Related Report
      2004 Annual Research Report
  • [Journal Article] Ischemic neuronal death and gap junctions.2003

    • Author(s)
      Oguro K, Tanaka H, Yokota H, Miyawaki T.
    • Journal Title

      Prevention and therapy for neuronal death by cerebrovascular disease (Kawai N ed.) Tokyo

      Pages: 109-128

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Book] 虚血性神経細胞死とギャップ結合in脳血管障害による「神経細胞死」の予防と治療(河合述史編集)2003

    • Author(s)
      小黒恵司, 田中秀信, 横田英典, 宮脇貴裕
    • Publisher
      クバプロ
    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Book] 虚血性神経細胞死とギャップ結合in脳血管障害による「神経細胞死」の予防と治療(川合述史編)2003

    • Author(s)
      小黒恵司, 田中秀信, 横田英典, 宮脇貴裕
    • Publisher
      クバプロ
    • Related Report
      2004 Annual Research Report
  • [Publications] Oguro K, Miyawaki T, Yokota H, Kato, M, Watanabe M, Shimazaki K, et al.: "Upregulation of GluR2 decreases intracellular Ca^<2+> following ischemia in developing gerbils"Neurosci.Letter. (in press). (2004)

    • Related Report
      2003 Annual Research Report
  • [Publications] 小黒恵司, 田中秀信, 横田英典, 宮脇貴裕: "虚血性神経細胞死とギャップ結合 in 脳血管障害による「神経細胞死」の予防と治療"川合述史編集(クバプロ). 109-128 (2003)

    • Related Report
      2003 Annual Research Report

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Published: 2003-04-01   Modified: 2016-04-21  

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