| Project/Area Number |
20500370
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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 |
Laboratory animal science
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| Research Institution | Nagoya University |
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Principal Investigator |
TAKAGISHI Yoshiko Nagoya University, 環境医学研究所, 助教 (50024659)
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| Co-Investigator(Kenkyū-buntansha) |
ODA Senーichi 岡山理科大学, 理学部, 教授 (60023660)
HAYASHI Yoshitaka 名古屋大学, 環境医学研究所, 准教授 (80420363)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 疾患モデル / 有髄神経線維 / ミエリン / 軸索 / 突然変異マウス / 髄神経線維 / ランビエ絞輪 / パラノード / 免疫組織化学 / 電子顕微鏡学 |
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| Research Abstract |
The shambling (shm) mouse with mutation of a Caspr gene exhibits ataxia and hind limb paresis at 2～3 weeks of age after birth. Caspr is a major component of the paranode in myelinated nerves. Disrupted paranodal junctions and aberrant localization of ion channels at the nodal/paranodal regions were found in the central and peripheral nervous system of mutant mice, suggesting a major cause of the mouse neurological phenotype. In aged mice showing progressive neurological deficits, altered axons containing abnormal inclusions and, further, a loss of neuronal somata were found. These findings suggest that the disrupted paranodal junction at the paranode causes the axonal degeneration and neuronal cell death, thus the shm mice is a potential animal model for human neurodegenerative disease.
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