| Project/Area Number |
10470326
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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 | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
ISSIKI Atsusi Tokyo Medical University, Anesthesiology, Professor, 医学部, 教授 (60074796)
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| Co-Investigator(Kenkyū-buntansha) |
OGIWARA Yukihiko Tokyo Medical University, Anesthesiology, Assis Prof, 医学部, 講師 (40224141)
OUMI Akifumi Tokyo Medical University, Anesthesiology, Assis Prof, 医学部, 講師 (70246221)
WATANABE Yasuo Tokyo Medical University, Pharmacology, Assos Prof, 医学部, 助教授 (70183720)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1999: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | CaィイD12+ィエD1 / L-type CaィイD12+ィエD1 channel / T-type CaィイD12+ィエD1 channel / pain / cyclooxygenase II / spinal neuron / GABAa receptor / GABAb receptor / flinching / 電位依存性Ca^<2+>チャンネル / 疼痛制御機構 / 二次性疼痛 / c-fos / Bcl-2 / L型 / T型 / 腰髄 |
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| Research Abstract |
In the neuronal pathway of the spinal cord, L- and T-type CaィイD12+ィエD1 channels, cyclooxygenase(COX) isozyme and GABA receptor subtype play important roles in pain regulation. In this experiment, we compared the effects of intralthecal injections of above specific inhibitors on secondary nociception induced by formalin using male Wistar rats(about 300g). As specific inhibitors, nimodipine(L-type), flunarizine(T-type), NS398(COX II), muscimol(GABAa) and baclofen(GABAb) were used.All agents were abministered intranthecally 10 min prior to formalin injection.Flinching was quantified in five minute intervals for 60min. These inhibitors significantly blocked formalin-induced pain. Particularly, intrathecal injection of flunarizine/baclofen showed the strong inhibition. Flunarizine also suppressed the appearance of c-fos induced by formalin. However, the larger dosage of NS398, which partially suppressed COX I, did not show any inhibition on formalin-induced pain. This NS398 dosage enhanced the nociceptive response. In conclusion, the prostanoid synthetic pathway activated by cytosolic CaィイD12+ィエD1 via T-type channel in the spinal cord appears to strongly influence nociceptive response, and the physiological balance between COX I and II activities may be associated with the regulation of prostanoid synthesis and GABAb receptor.
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