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Mechanisms of microglial stress response in injured central nervous tissue

Research Project

Project/Area Number 12671341
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Cerebral neurosurgery
Research InstitutionChiba University

Principal Investigator

YAMAURA Akira  Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (40009717)

Co-Investigator(Kenkyū-buntansha) YAMAKAMI Iwao  Chiba University, University Hospital, Lecturer, 医学部・附属病院, 講師 (90241968)
SAEKI Naokatu  Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 助教授 (30143275)
MURAI Hisayuki  Chiba University, University Hospital, Assistant, 医学部・附属病院, 助手 (80241967)
IWADATE Yasuo  Chiba University, Graduate School of Medicine, Assistant, 大学院・医学研究院, 助手 (70272309)
久保田 基夫  千葉大学, 医学部・附属病院, 助手 (10225211)
Project Period (FY) 2000 – 2001
Project Status Completed (Fiscal Year 2001)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥2,200,000 (Direct Cost: ¥2,200,000)
Keywordstraumatic brain injury / microglia / astroglia / immunotoxin / neuron / 頭部外傷 / 脳挫傷
Research Abstract

As a whole, whether activated microglia are acting as protectors or attackers to the neurons in response to the certain pathological condition such as trauma? In this study we used microglia-specific immunotoxin, Mac-1-SAPORIN, at the time of injury to temporally eliminate microglia to see the effects following penetrating traumatic brain injury in mice.
At 24 hours after injury, very few arborized microglia were observed around the injury site in microglia ablation group, while arborized microglia were widely distributed around the injury site or throughout the ipsilateral hippocampus and round-shaped microglia/macrophage were sparsely distributed along the needle track in microglia non-ablation group. At 7 days after injury, many arborized microglia were observed around the injury site or throughout the ipsilateral hippocampus even in immunotoxin treated (microglia ablation) group. Gliosis around the injury site was more evident in microglia non-ablation group at 72 hours and 7 days following injury. At 72 hours after injury, the neuronal cell loss became evident in the non-ablation group compared to that in ablation group. However, at 7 days after injury, no statistically significant difference was observed.
The microglia ablation with immunotoxin ameliorated the neuronal cell loss in the dentate gyrus following penetrating traumatic brain injury in the mouse hippocampus. The microglia ablation also inhibited the hypertrophic change and proliferation of astrocytes following traumatic brain injury. We concluded that activated microglia in the acute stage of penetrating brain injury are considered to mainly act on the neurons suffering from injury as attackers through their phagocytic function and/or modification of astrocyte-neuron interaction.

Report

(3 results)
  • 2001 Annual Research Report   Final Research Report Summary
  • 2000 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] 枝美絵子, 大賀優, 村井尚之, 山浦 晶: "外傷後神経損傷過程におけるmicrogliaの総括的役割の推定-Immunotoxinを用いた実験的検討-"Neurologica medico-chirurgica. 41(extra issue). 374 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] Eda M, Ohga M, Murai H, Yamaura A: "The effects of microglia ablation following traumatic brain injury in mice"Neurologia medico-chirurgica. 41 extra issue. 374 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2001 Final Research Report Summary
  • [Publications] 枝美絵子, 他: "外傷後神経損傷過程におけるmicrogliaの総括的役割の推定-Immunotoxinを用いた実験的検討-"Neurologica medico-chirurgica. 41・extra issue. 374 (2001)

    • Related Report
      2001 Annual Research Report

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Published: 2000-04-01   Modified: 2016-04-21  

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