| Project/Area Number |
61480441
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
応用薬理学・医療系薬学
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| Research Institution | Kyoto University |
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Principal Investigator |
SATOH Masamichi Kyoto Univ.,Fac. of Pharm. Sci.,Dept. of Pharmacol.:Professor, 薬学部, 教授 (80025709)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 1987: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1986: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | Chronic pain / Adjuvant arthritic rat / Neuropeptide / Substance P / Calcitionin qene-related peptide / Spinal dorsal horn / Primary afferent / 鎮痛薬 / アジュバント関節炎ラット / 後根神経節 / コルヒチン |
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| Research Abstract |
I used polyarthritic rats as a model of chronic pain and reveaied the following points concerning the turnover change of a neuropeptide, substance P, which is involved in nociceptive transmission in the spinal dorsal horn, in the rats and an influence of an analgesic on the change.
1) The content of immunoreactive substance P (iSP) in the dorsal root ganglia of L4 and L5 was significantly higher in polyarthritic rats than in control rats. On the contrary, that in the dorsal horn was lower in the former than in the latter.
2) The treatment with colchicine, a blocker of axonal flow, produced a further increase in the content of iSP in the dorsal root ganglia of polyarthritic rats, but did not significantly change that of control rats.
3) The spontaneous release of iSP from the spinal dorsal horn was enhanced in polyarthritic rats.
4) Systemic administration of morphine which inhibits the release of iSP from the dorsal horn increased the content of iSP in the dorsal horn only in polyarthritic ratrs. These findings suggest that the biosynthesis, axonal flow and release from the primary afferent terminals of substance P are enhanced in polyarthritic arts, and that morphine inhibits the release of substance P.
5) Intrathecal injection of calcitonin gene-related peptide (CGRP) produced a hyoperalgesia to mechanical noxious stimuli in control and polyarthritic rats. But the degree of the hyperalgesia was larger in the latter than in the former. Such an effect of CGRP was inhibited by a substance P antagonist. These results suggest an involvement of CGRP in the transmission of chronic pain in the rat spinal dorsal horn.
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