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Dissecting the mechanism of sensory neuron sensitization for the treatment of chronic pain

Research Project

Project/Area Number 15591655
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Anesthesiology/Resuscitation studies
Research InstitutionKyoto Prefectural University of Medicine

Principal Investigator

TANAKA Yoshifumi (2004)  Kyoto Prefectural University of Medicine, Department of Anesthesiology, Professor, 医学研究科, 教授 (50079935)

天谷 文昌 (2003)  京都府立医科大学, 医学研究科, 助手 (60347466)

Co-Investigator(Kenkyū-buntansha) TANAKA Masaki  Kyoto Prefectural University of Medicine, Department of Anatomy, Associate professor, 医学研究科, 助教授 (80264753)
SHIME Nobuaki  Kyoto Prefectural University of Medicine, Department of Anesthesiology, Assistant professor, 医学研究科, 助手 (00260795)
KAGEYAMA Kyoko  Kyoto Prefectural University of Medicine, Department of Anesthesiology, Assistant professor, 医学研究科, 助手 (80347468)
田中 義文  京都府立医科大学, 医学研究科, 教授 (50079935)
Project Period (FY) 2003 – 2004
Project Status Completed (Fiscal Year 2004)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2003: ¥2,200,000 (Direct Cost: ¥2,200,000)
KeywordsInflammation / Hyperalgesia / VR-1 / VRL-1 / NGF / GDNF / DRG / Rat / VR1 / 免疫組織化学
Research Abstract

Capsaicin Receptor, VR-1 and its homologue VRL-1 are cation channels and expressed primary afferent neurons to mediate noxious thermal stimulation. To specialize their role for the sensitization of primary afferent, we conducted some experiments as follows.
1)Histochemical analysis of VR-1 and VRL-1 following inflammation
We performed immunohistochemistry against VR-1/VRL-1 in rat DRG. We measured the number of primary afferent neurons that express VR-1 or VRL-1. Peripheral inflammation increased expressions of both VR-1 and VRL-1.
2)Measurement of neurotrophic factor, NGF and GDNF within the dorsal root ganglion(DRG)
We determined the level of NGF and GDNF within the DRG by ELISA. Both level increased by the inflammation.
3)Effect of anti-NGF or anti-GDNF on the expression of VR-1/VRL-1 as well as behavioural hyperalgesia following inflammation.
Pre-treated with anti-NGF and anti-GDNF can prevent development of thermal hyperalgesia induced by the inflammation. Treatment with both factor inhibited inflammatory VR-1 expression but not VRL-1.
These results suggest that induction of VR-1/VRL-1 can facilitate heat hyperalgesia induced by the inflammation. Nerve trophic factor regulate inflammatory VR-1 expression but not VRL-1.

Report

(3 results)
  • 2004 Annual Research Report   Final Research Report Summary
  • 2003 Annual Research Report
  • Research Products

    (1 results)

All 2004

All Journal Article (1 results)

  • [Journal Article] NGF and GDNF differentially regulate TRPV1 expression that contributes to development of inflammatory thermal hyperalgesia.2004

    • Author(s)
      Amaya F, Shimosato G, Nagano M, Ueda M, Hashimoto S, Tanaka Y, Suzuki H, Tanaka M.
    • Journal Title

      European Journal of Neuroscience 20(9)

      Pages: 2303-2310

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Annual Research Report 2004 Final Research Report Summary

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Published: 2003-04-01   Modified: 2016-04-21  

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