Dissecting the mechanism of sensory neuron sensitization for the treatment of chronic pain
Grant-in-Aid for Scientific Research (C)
|Allocation Type||Single-year Grants|
|Research Institution||Kyoto Prefectural University of Medicine|
TANAKA Yoshifumi(2004) Kyoto Prefectural University of Medicine, Department of Anesthesiology, Professor, 医学研究科, 教授 (50079935)
天谷 文昌 京都府立医大, 医学系研, 助手 (60347466)
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
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)
|Keywords||Inflammation / Hyperalgesia / VR-1 / VRL-1 / NGF / GDNF / DRG / Rat / VR1 / 免疫組織化学|
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.
Research Products (1results)