| Project/Area Number |
24791979
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional basic dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | ミクログリア / BKチャネル / モルヒネ / 痛覚過敏 / 疼痛過敏 / 国際情報交換 |
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| Outline of Final Research Achievements |
We have found that BK channels in the spinal microglia contribute to the initiation of neuropathic pain. In the present study, we have examined a possible involvement of microglial BK channels in opioid-induced hyperalgesia (MIH), because some evidence suggests the involvement of microglia in this event. Repeated morphine administration gradually enhanced pain sensitivity. At the same time, repeated morphine administration activated BK channels in microglia, but not in neuron, by generation of arachidonic acid and its metabolites through mu receptors. MIH was significantly suppressed by BK channel inhibitor. The development of hyperalgesia was accelerated by intrathecal administration of morphine-primed wild-type, but not BK channel-deficient, microglia. Furthermore, the activation of BK channels promoted P2X4 receptor trafficking to the cell surface of microglia. These results indicate that BK channels in the spinal microglia also play an important role in the development of MIH.
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