| Project/Area Number |
11835009
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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 Institution | Chiba University |
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Principal Investigator |
YOSHINAGA Kasunori Chiba University, University Hospital, Assistant Professor, 医学部・附属病院, 助教授 (30270870)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Masazumi Chiba University, School of Medicine, Assistant, 医学部, 助手 (50219903)
YAMAZAKI Masashi Chiba University, University Hospital, Assistant, 医学部・附属病院, 助手 (50281712)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Spinal cord injury / brain-derived neurotrophic factor / neurotrophin-3 / neurotrophin-3(NT-3) |
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| Research Abstract |
BDNF and NT-3, members of the NGF family of trophic factors, have multiple functions including a role in the promotion of neuronal survival and nerve fiber elongation in both the CNS and the PNS.We assessed the expression of endogenous BDNF and NT-3 following an experimentally-induced compression injury to the spinal cord. Expression of BDNF mRNA was increased following the spinal cord injury ; reaching maximum levels 24 hr after the injury. Expression of BDNF mRNA returned to the levels observed in sham-operated control antimals within 3 days of the injury. In contrast, NT-3 mRNA was up-regulated 1 week after the injury and reached to the peak level 2 weeks after the trauma. Using the in situ hybridization technique, we observed a wide distribution of BDNF and NT-3 expression amongst the different cell types in the spinal cord including motor and sensory neurons, and in glial cells, including astrocytes and oligodendrocytes. These results suggest that BDNF is synthesized in both neurons and glial cells during the acute response to injury to the spinal cord, functioning in a mainly neuroprotective role. This is followed by a later phase of NT-3 expression in neurons and glial cells, functioning in a restorative capacity. Especially, NT-3 expression in oligodendrocytes in the later phase suggests that this factor supports restration of long tracts.
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