| Project/Area Number |
17580268
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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 |
Applied veterinary science
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
KUWAMURA Mitsuru Osaka Prefecture University, Graduate School of Life & Environmental Sciences, Lecturer (20244668)
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| Co-Investigator(Kenkyū-buntansha) |
TAKENAKA Shigeo Osaka Prefecture University, Graduate School of Life and Environmental Science, Associate Professor (10280067)
YAMEATE Jyoji Osaka Prefecture University, Graduate School of Life and Environmental Science, Associate Professor (50150115)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | demvelination / myelin / regeneration / neural stem cell |
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| Research Abstract |
The myelin vacuolation (my) rat is an autosomal recessive mutant characterized by hypomyelination and vacuole formation in the myelin throughout the central nervous system (CNS). Previous genetic studies have revealed a null mutation in attractin gene of the my mutant rat. It has been known that mutation at the attractin locus results in myelin alterations, but their detailed pathogenesis is still unclear. In this study, we examined glial changes in the spinal cord of my rats at 2, 4, 6, 8 weeks of age and identified attractin-expressing cells in the rat spinal cord.
No abnormality was found in the number and morphology of oligodendrocytes in my rats at any of the ages examined, although the severity and extent of myelin disorder increased with age. Coincident with the myelin abnormalities, there was progressive astrogliosis from 2 weeks. Marked microglial activation was observed exclusively in the gray matter of my rats from 6 weeks, coincident with severe myelin disruption. A double-labeling study demonstrated that attractin-expressing cells in the spinal cord are mostly oligodendrocytes in wild-type rats, whereas no attractin-positive cells were detected in my rats.
These findings indicate that the attractin defect results in oligodendrocyte dysfunction, and is associated with astrogliosis and microglial activation in my rats. The data suggest that attractin may be directly involved in the function of oligodendrocytes in CNS myelination.
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