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The role of Fc receptors in microglial activation and excototoxic neuronal death.

Research Project

Project/Area Number 16591140
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Psychiatric science
Research InstitutionOkayama University

Principal Investigator

OKAMOTO Motoi  Okayama University, Medical School, Professor, 医学部, 教授 (80144757)

Co-Investigator(Kenkyū-buntansha) ISHIKAWA Tetsuya  Okayama University, Medical School, Assistant Professor, 医学部, 助教授 (90221754)
USUI Shinichi  Okayama University, Medical School, Assistant, 医学部, 助手 (50346417)
SATO Hiaki  Okayama University, Medical School, Assistant, 医学部, 助手 (70362960)
Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
Keywordsexcitotoxic neuronal death / mouse / kainic acid / hippocampus / pyramidal cell loss / FcR-deficient mouse / microglia / astrocyte / Fc受容体 / 遺伝子欠損 / 局所注入 / 錐体細胞死
Research Abstract

The role of IgG Fc receptors in microglial activation and excitotoxic neuronal death was examined in the mouse deficient of γ subunit of FcγRIII (FcRγ-/-), or FcγRIIB (FcγRIIB-/-). Both FcRγ-/- and Fc γRIIB-/- were extremely sensitive to systemic administration of kainic acid (KA) as well as wild type mouse C57BL/6J. However, the duration of convulsive status was significantly shorter in FcR-deficient mouse than C57BL/6J. In addition, appearance of activated microglia and reactive astrocyte was poor in FcR-deficient mousse suggesting that Fc receptors contribute to maintenance of convulsive seizures and activation of microglia and astrocyte.
In FcR-deficinet mouse, pyramidal cell loss following intrahippocampal KA injection was significantly mild compared to C57BL/6J in which moderate pyramidal cell loss occurred within 24 hours following KA injection. Because expression of IL-6,IL-1β,TNF-α reached a peak at 4 hours after KA injection in FcR-deficient mouse whereas IL-6,IL-1β were more persistently expressed in C57BL/6J, Fc receptors contribute to regulation of cytokine expression and hence pyramidal cell loss following excitotoxic stimuli. In addition, primary culture of mouse forebrain neurons and astrocyte has been established to investigate molecular mechanism of the role of Fc receptors and microglia.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report

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Published: 2004-04-01   Modified: 2016-04-21  

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