The role of glycine in neuronal injury after spinal cord injury
| Project/Area Number |
22591603
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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 |
Cerebral neurosurgery
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| Research Institution | Akita University |
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Principal Investigator |
SUGAWARA Taku 秋田大学, 大学院・医学系研究科, 講師 (80241660)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 脊髄損傷 / 運動ニューロン / アポトーシス / DNA損傷 / グリシン / ＤＮＡ損傷 |
|---|
| Research Abstract |
Ventral horn motor neurons (VMN) are selectively vulnerable to mild spinal cord injury (SCI); however, the mechanisms of cell death had not been understood. To clarify the role of glycine in SCI, mild compression SCI was induced in normal C57BL/6 mice, extracellular low glycine concentration mice and high glycine concentration mice. A majority of VMN (80%) selectively underwent delayed apoptotic cell death. However, there were no difference in the extent of cell injury and apoptotic changes in those three groups. Further studies are needed to clarify the role of glycine in apoptotic motor neuronal death after mild SCI.
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Report
(4 results)
Research Products
(44 results)
