| Project/Area Number |
18591703
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Okayama University |
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Principal Investigator |
SATO Tetsufumi Okayama University, University Hospital of Medicine & Dentistry, Assistant Proressor (40362975)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOYAMA Masataka Okayama University, Graduate School of Medicine, Dentistry & Pharmaceutical Science, Associate Professor (20158380)
ITANO Yoshitaro Okayama University, Graduate School of Medicine, Dentistry & Pharmaceutical Science, Assistant professor (30127542)
MORITA Kiyoshi Okayama University, Graduate School of Medicine, Dentistry & Pharmaceutical Science, Professor (40108171)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,920,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | siRNA / Brain-derived neurotrophic factor (BDNF) / Intractable vain / Exon / Gene therapy / 脳由来神経栄養因子 / 鎮痛法 / 遺伝子療法 |
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| Research Abstract |
We tried to control pain by knocking-down BDNF exon with siRNA. To investigate which exon of BDNF is involved in inflammatory pain and neuropathic pain, we quantitated inflammation-induced (CFA) and nerve injury-induced (L5 spinal nerve ligation) expression of BDNF exons in the rat DRG by PCR. We also investigated changes in expression of BDNF splice variants in cultured DRG neurons exposed to NGF.
Total BDNF mRNA was increased by inflammation and nerve injury in vivo and by NGF in vitro. Among all splice variants, exon I showed the greatest increase in expression in both experiments.
Therefore, we targeted the exon I of BDNF for knock-down with siRNA. We created the two different siRNAs for exson I of BDNF. The two different siRNAs for the exon I of BDNF were administered intrathecally in CFA-induce pain rats. The pain behaviors were decreased by the administration of siRNAs, but not completely suppressed. The expression of BDNF was not completed suppressed in DRG after the administration of the two siRNAs. We performed same experiments in different doses of siRNA and different timing for administration, but analgesic effects were similar.
Our results indicate that siRNA for the exon I of BDNF has only little analgesic effects.
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