2002 Fiscal Year Final Research Report Summary
Neuronal and behavioral research on the function of ATP receptors in the signal trasnduction of pain.
| Project/Area Number |
11557115
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | National Institute of Health Sciences (NIHS) |
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Principal Investigator |
INOUE Kazuhide NIHS BIOSIGNALING DIRECTOR, 代謝生化学部, 部長 (80124379)
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| Co-Investigator(Kenkyū-buntansha) |
KOIZUMI Schuichi NIHS PHARMACOLOGY SECTION CHEAF, 薬理部, 室長 (10280752)
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| Project Period (FY) |
1999 – 2002
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| Keywords | ATP RECEPTOR / P2X / P2Y / NEUROPATHIC PAIN / ALLODYNIA / DRG / C-FIBER / Aδ |
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| Research Abstract |
We had found that the stimulation of ATP receptors evoked allodynia as well as nocifensive behavior and hyperthermal algesia. This allodynia is similar to the symptom of neuropathic pain which is resistant to morphine and NSAIDs, anti-pain drugs. To control of this pain is very important in the clinical event, we tried to reveal the mechanism and find the responsible receptor subtype. In the project we found that the both stimulation of ionotropic P2X receptor and G protein-coupled receptor P2Yevoke novel allodynia-like behaviors which are different from each other mentioned below.
The stimulation by α,βmethlene ATP of P2X2+3 heteromeric receptor ( P2X2 and P2X3 compose a heteromeric origomer which is a novel functional receptor/channel.) caused the allodynia which is independent of C-fiber and is continue to 2 hr after the stimulation. On the other, the stimulation of P2Y2 caused C-fiber dependent allodynia which is continue to more than 4 hr after the stimulation. These results indicate that both allodynia are evoked a different mechanism, respectively.
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[Publications] T.Moriyama, T. Iida, K. Kobayashi, T. Higashi, T. Fukuoka, H. Tsumura, C. Leon, N. Suzuki, K. Inoue , C. Gachet, K. Noguchi and M. Tominaga: "Possible involvement of P2Y2 metabotropic receptors in ATP-induced TRPV1-mediated thermal hypersensitivity"Pro.Natl.Acad.Sci.USA,. in press.
Description
「研究成果報告書概要(欧文)」より
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