2016 Fiscal Year Final Research Report
Elucidation of mechanism of neuropathic pain using acromelic acid A-induced allodynia model
Project/Area Number |
25462456
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Anesthesiology
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Research Institution | Osaka Medical College |
Principal Investigator |
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Co-Investigator(Renkei-kenkyūsha) |
FURUTA Kyoji 岐阜大学, 医学(系)研究科(研究院), 准教授 (40173538)
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Project Period (FY) |
2013-04-01 – 2017-03-31
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Keywords | 神経障害性疼痛 / アロディニア / グルタミン酸受容体 / アクロメリン酸 / アストロサイト / ミクログリア |
Outline of Final Research Achievements |
We previously showed that intrathecal administration of acromelic acid A (ACRO-A) provoked tactile allodynia in mice. In order to clarify their involvement in ACRO-A-induced allodynia, we investigated the effects of various agents at early and late-phase allodynia. All of agents (Ca2+ channel α2δ ligands, NMDA and AMPA receptor antagonists, nNOS, and Ca2+/calmodulin kinase II inhibitors) blocked allodynia in the early-phase group; however, they did not block allodynia in the late-phase group. In order to block glial activation, astrocytic inhibitor LAA or microglia linhibitor minocycline was administrated. Microglial activation was observed 1week after ACRO-A injection and was significantly inhibited with minocycline treatment. Moreover, only LAA was found to inhibit late-phase allodynia. We demonstrate that NMDA receptor activation is involved only in ACRO-A-induced allodynia in the early phase, and that spinal astrocytic activation contributes to allodynia in the late phase.
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Free Research Field |
疼痛治療学
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