| Project/Area Number |
13470039
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Kansai Medical University |
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Principal Investigator |
ITO Seiji Kansai Medical University, Faculty of Medicine, Professor, 医学部, 教授 (80201325)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUMURA Shinji Kansai Medical University, Faculty of Medicine, Instructor, 医学部, 助手 (70276393)
YAMADA Hisao Kansai Medical University, Faculty of Medicine, Professor, 医学部, 教授 (00142373)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥9,700,000 (Direct Cost: ¥9,700,000)
Fiscal Year 2002: ¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 2001: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | spinal cord / neuropathic pain / transgenic mice / neural stem cell / nestin / GFP / nitric oxide / 神経再生 / ネスチン / 後根神経節 |
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| Research Abstract |
The present study focused on the role of neural regeneration and reorganization of neural circuit in induction of tactile pain (allodynia) by use of pNestin-GFP transgenic mice, which are introduced by a transgene of green fluorescent protein (GFP) driven by a promotor of nestin, an intermediate filament expressed in neural stem cells. To induce allodynia, we established a neuropathic pain model in mice by selective 5^<th> lumbar spinal nerve transection, in addition to intrathecal injection model previously established.
We extensively examined the expression of GFP in dorsal root ganglia (DRG) and spinal cord in embryos to adult mice. In whole embryos, the intense expression of GFP was observed around central canals over the spinal cord, which was gradually decreased after birth. This expression around the central canal was confirmed by the lumbar slice. In DRG neurons, GFP was strongly expressed in pericytes, rather than neurons themselves. In neuropathic mice, GFP-positive cells bilaterally increased in the dorsal horn on days 2 and 3 after operation. Following subsidence of inflammation, neuropathic pain was established in the ipsilateral side to the operation and the number of GFP-positive cells was significantly larger in the ipsilateral side than in the contralateral side. These cells were not stained by antibodies specific for neurons and astrocytes. In parallel, we showed that nitric oxide synthase activity was increased around the central canal in neuropathic mice. This finding may imply that the relationship between noxious inputs from the periphery to the central canal and chronic pain or neural plasticity. At present, in order to clarify where neural stem cells proliferate, to where they migrate, and how they differentiate into neurons and glias, the mechanism of activation and the pathway of migration of neural stem cells are under investigation.
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