| Project/Area Number |
12672233
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
応用薬理学・医療系薬学
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| Research Institution | KINKI UNIVERSITY |
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Principal Investigator |
KURODA Ryotaro KINKI UNIVERSITY, DEPT. OF PATHOPHYSIOLOGY FAC. OF PHARMCEUT SCI., PROFESSOR, 薬学部, 教授 (10161803)
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| Co-Investigator(Kenkyū-buntansha) |
KAWABATA Atsufumi KINKI UNIVERSITY, DEPT. OF PATHOPHYSIOLOGY FAC. OF PHARMCEUT. SCI., ASSOCIATE PROFESSOR, 薬学部, 助教授 (20177728)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | PAR-2 / cortical stimulation / analgesia / hyperalgesia / nociceptive behavior / Fos / NMDA / NO / 第2次体性感覚野 / 電気刺激 / c-Fos / 7-ニトロインダゾール / ホルマリン疼痛 |
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| Research Abstract |
The aim of the study was to establish novel animal models in which electrical stimulation of cortical Sll area, known to be clinically analgesic, is capable of producing potent antinociception.
1. Sll stimulation-evoked antinociception in the formalin-induced nociception model : Stimulation electrodes were chronically implanted into the Sll area of the rat. The formalin-induced nociceptive behavior and expression of Fos in the superficial layer of the dorsal horn was slightly reduced by Sll stimulation. Sll stimulation in combination with 7-nitro indazole, a neuronal NO synthase inhibitor, produced strong antinociception and suppression of Fos expression. The effect of Sll stimulation was partially blocked by intrathecal administration of methysergide, a serotonin receptor antagonist, suggesting involvement of the descending serotonin neurons.
2. PAR-2-triggered nociception model and its characterization : Stimulation of PAR-2 expressed in the peripheral terminal of C-fiber triggered thermal hyperalgesia, nociceptive behavior and expression of spinal Fos. The nociceptive processing by PAR-2 was characterized in the present study.
3. Effect of Sll stimulation in the PAR-2-mediated nociception model and the surgically prepared neuropathy model : Sll stimulation failed to exhibit any antinociceptive activity in these two models.
Further effort will be necessary to establish models in which Sll stimulation is highly analgesic.
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