| Project/Area Number |
21591908
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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 |
Orthopaedic surgery
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MIYOSHI Kan 兵庫医科大学, 医学部, 助教 (30454755)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 脊椎脊髄病学 / IL-18 / TLR4 / MAPK / グリア細胞 / 神経障害性疼痛 / 坐骨神経痛 |
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| Research Abstract |
In order to investigate the molecular mechanisms of pain seen in orthopedic clinics, such as root injury/compression pain, we have used two rat models of root injury-induced pain. One is ventral root injury model and another is dorsal root injury model. We examined the pain behaviors of these two models and found that the ventral root injury model showed more stable hyperalgesia and allodynia compared to dorsal root injury model. Using immunohistochemistry with antibodies for Iba-1 and GFAP, we found that activation of glial cells(microglia and astrocyte) in the spinal cord even after ventral root injury. We also confirmed that phosphorylated ERK was increased in the spinal cord in the ventral root injury model, which might have a role in ventral injury-induced pain hypersensitivity. With collaboration with a laboratory in USA, we published a paper in J. Neurosci, where the finding that neuro-glial interaction is important in descending pain accelerating pathway in the spinal cord, was presented.
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