| Project/Area Number |
13670032
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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 |
General anatomy (including Histology/Embryology)
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| Research Institution | Hyogo College of Medicine |
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Principal Investigator |
DAI Yi Hyogo College of Medicine, research associate, 医学部, 助手 (20330441)
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| Co-Investigator(Kenkyū-buntansha) |
NOGUCHI Koichi Hyogo College of Medicine Professor, 医学部, 教授 (10212127)
TOKUNAGA Atsushi Hyogo College of Medicine Associate Prof, 医学部, 講師 (70254521)
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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 |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Neuropathic pain / Gene expression / Dorsal root ganglion / BDNF / Substance P / NGF / GDNF / ラット / 脊髄神経 |
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| Research Abstract |
We examined the effect of L5 spinal nerve ligation (SPNL), a neuropathic pain model, on the expression of EDNF in the uninjured L4 dorsal root ganglion (DRG). A significantly greater number of BDNF-immunoreactive neurons were observed in the ipsilateral L4 DRG than contralateral side 14 days after ligation. The percentage of BDNF mRNA-expressing cells of trkA cells significantly increased in the ipsilateral L4 DRG 14 days after ligation. Further, NGF content in the ipsilateral L4 DRG linearly increased. Local application of anti-NGF antibody to the L4 spinal nerve beside the L5 spinal nerve-ligation site prevented the development of thermal hyperalgesia for 5 days after ligation. These data suggest that BDNF, which increased in the uninjured L4 DRG neurons, acts as a sensory-neuromodulator in the dorsal horn and contributes to thermal hyperalgesia in this neuropathic pain model.
We also found that x the content of mRNA for substance P in uninjured trigeminal ganglion neurons increased following the transection of infraorbital nerve.
These data suggest that in neuropathic pain models there are significant alteration of expression of pain-related molecules such as BDNF or Substance P in uninjured primary afferent neurons and these changes are supposed to be important pathomechanisms of neuropathic pain.
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