| Project/Area Number |
16500362
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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 |
Rehabilitation science/Welfare engineering
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| Research Institution | The Jikei University School of Medicine |
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Principal Investigator |
ABO Masahiro The Jikei University School of Medicine, lecturer, 医学部, 講師 (00266587)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAUCHI Hideki The Jikei University School of Medicine, lecturer, 医学部, 講師 (60220224)
浦島 充佳 東京慈恵会医科大学, 医学部, 講師 (80203602)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | stroke / rat / reorganization / Gene Chip / Kynurenic acid / Glycine receptor / Glutamate receptor / muscle evaluation / GeneChip / Rose-Bengal / Beam-walking / DNAチップ |
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| Research Abstract |
The aim of this study was to assess skeletal muscle showing a complete functional recovery after induction of pan-necrotic lesions in the right sensorimotor cortex in rats. All Stroke group rats showed complete functional recovery in the beam-walking test within 10 days. The score of the sham-operated group rats was 7 for 21 days. The wet weight of the soleus muscle (SOL) only in the Stroke group and Stroke plus severed right sciatic nerve group was significantly greater than in the sham-operated group. The cross-sectional area of type I fibres was increased in SOL. It was concluded that the functional recovery was mainly due to increased wet weight and cross-sectional area of type I SOL fibres, which probably reflected the functional reorganization and neuromodulation in the non-damaged contralateral sensorimotor cortex and ipsilateral sensorimotor cortex lateral to the lesion identified in a previous study.
Therefore, we next aimed to find key molecules upregulated in those activated
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area using gene expression pro filing as a screening tool in this experiment. Using the same rat model of brain infarction by photochemically initiated thrombosis, RNA was extracted from ipsilateral and contralateral sensorimotor cortex to the focal brain infarction as well as control cortex were hybridized with gene expression pro filing arrays containing 1,322 genes. As a result, NMDA receptor was screened as a candidate for further experiment, since glycine and glutamate receptors were upregulated in both ipsilateral and contralateral cortex to focal ischemic lesion, which were also confirmed by immunohistochemical staining. Intrathecal administration of kynurenic acid, an endogenous antagonist to NMDA receptor, facilitated behavioral recovery from paralysis triggered by focal photothrombotic ischemic brain lesion (P<0.0001). These results suggest that altered expression of NMDA receptor screened with the GeneChip may delay, at least in part, behavioral recovery during acute phase after brain infarction. Less
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