| Project/Area Number |
11680782
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neuroscience in general
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
FUKAMAUCHI Fumihiko Medical Research Institute Tokyo Medical and Dental University, 難治疾患研究所, 助教授 (90240746)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Kazutada Tokyo Metropolitan Inst. of Gerentology., 細胞認識部門, 室長 (70114717)
IWAKURA Yoichiro University of Tokyo, Inst. of Medical Sci, Professor, 医科学研究所, 教授 (10089120)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1999: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | TAG-1 / Gene targeting / Knockout mouse / axon guidance / Adenosine / 免疫グロブリンスーパーファミリー / アデノシン |
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| Research Abstract |
TAG-1 is a neural recognition molecule in the immunoglobulin superfamily that is predominantly expressed in the developing brain. Several lines of evidence suggest that TAG-1 is involved in the outgrowth, guidance and fasciculation of neurites. To directly assess the function of TAG-1 in vivo, we have generated mice with a deletion in the gene encoding TAG-1 using homologous recombination in embryonic stem cells. Gross morphological analysis of the cerebellum, the spinal cord and the hippocampus appeared normal in TAG-1-deficient mice. However, TAG-1 (-/-) mice showed the upregulation of the adenosine A1 receptors determined by [^3H] cyclopentyl-1,3- dipropylxanthine in the hippocampus, and their greater sensitivity to convulsant stimuli than that in TAG-1 (+/+) mice. We suspect that the subtle changes in neural plasticity induced by TAG-1 deficiency during development cause the selective vulnerability of specific brain regions and the epileptogenicity in TAG-1 (-/-) mice.
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