| Project/Area Number |
10672164
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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, Faculty of Pharmaceutical Sciences, Professor, 薬学部, 教授 (10161803)
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| Co-Investigator(Kenkyū-buntansha) |
KAWABATA Atsufumi Kinki University, Faculty of Pharmaceutical Sciences, Lecturer, 薬学部, 講師 (20177728)
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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 |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | analgesia / cortical stimulation / pain / NO synthase inhibitor / c-fos / antinociception / secondary somatosensory cortex / NO / ホルマリン疼痛法 |
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| Research Abstract |
The primary aim of the present study was to establish an animal model in which analgesia could be produced by electrical stimulation of the secondary somatosensory cortex (S-II) that was clinically effective in a patient with intractable pain. We also wished to examine whether an inhibitor of neuronal nitric oxide (NO) synthase known to be involved in pain modulation could modify the S-II stimulation-produced analgesia.
S-II stimulation failed to induce antinociception in rats, as assessed by mechanical and thermal nociception test. However, it produced notable antinociception in the formalin-induced chemical nociception test. This antinociception by S-II stimulation was potentiated by 7-nitro-indazole (7-NI), an inhibitor of neuronal NO synthase. S-II stimulation in combination with 7-NI also suppressed the formalin-induced expression of c-fos in the superficial layers of the L4 and L5 spinal dorsal horn. The antinociception evoked by S-II stimulation plus 7-NI was resistant to systemic administration of naloxone, an opioid antagonist, or of phentolamine, an α-adrenoceptor antagonist, whereas the first phase, but not second phase, antinociception was significantly inhibited by intrathecal administration of methysergide, a serotonin receptor antagonist.
Our study suggests that S-II stimulation in combination with 7-NI produces strong antinociception by suppressing transmission of nociceptive information at a spinal level through activation of descending inhibitory pathways, especially serotonergic systems.
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