| Project/Area Number |
16500219
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Kobe University |
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Principal Investigator |
KIKKAWA Satoshi Kobe Univ., Grad.School of Med., Assistant professor, 大学院・医学系研究科, 助手 (90244681)
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| Co-Investigator(Kenkyū-buntansha) |
TERASHIMA Toshio Kobe Univ., Grad.School of Medicine, Professor, 大学院・医学系研究科, 教授 (20101892)
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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 |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | reelin / fukutin / pial membrane / glial limiting membrane / astroglia / zebrafish / gene knock-down / perforant pathway / 海馬裂 / 神経回路標識 |
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| Research Abstract |
We anterogradely labeled entorhinodentate axons in wild type and reeler mice at adult and neonatal stages. The results revealed that pioneer axons of the entrhinodentate tract develop similarly and pass through the hippocampal fissure at postnatal day 1(P1) in wild type and reeler mice. In the reeler mutant, however, follower axons can not pass through the fissure and detour around it, whereas those in wild type mice follow their pioneer and continue to pass through the fissure. Immunohistochemical analysis of postnatal development of the hippocampal area using anti-GFAP antibody demonstrated aberrant accumulation of GFAP-positive astroglia along the hippocampal fissure in the reeler but not wild type brain. This accumulation of astroglia seems to prevent the entorhinohippocampal axons from passing through the hippocampal fissure and forces them to detour along the fissure in the reeler mutant.
Next, we double-labeled neocortical neurons in the fukutin-deficient chimeric mouse with antero- or retro-grade axonal tracers and anti-laminin antibody to investigate relationship between collapse of the glial limiting membranes due to fukutin-deficiency and malpositioning of neocortical neurons. The results showed that a population of neocortical neurons positioned ectopically in the area just beneath the disrupted limiting membranes which lack laminin immunoreactivity, suggesting that the glial limiting membranes have certain effects on cortical neuronal migration.
Thirdly, we cloned and sequenced the complete coding region of zebrafish fukutin. Zebrafish fukutin showed a significant degree of sequence conservation. Fukutin mRNA was detected a wide variety of tissues including the brain and the spinal cord. We also tried knocking-down fukutin protein expression by antisense morpholino oligonucleotide microinjection into fertilized eggs. Further investigation of effects of fukutin knock-down on development of the central nervous system is currently being continued.
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