| Project/Area Number |
25462448
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Anesthesiology
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| Research Institution | Osaka City University |
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Principal Investigator |
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| Research Collaborator |
FANAI Yusuke 大阪市立大学, 大学院医学研究科, 大学院生 (60722486)
YAMASAKI Hiroyuki 大阪市立大学, 大学院医学研究科, 大学院生 (70759000)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 下行性抑制系 / in vivo patch clamp / 脊髄 / トラマドール / DSP-4 / 交感神経 / デクスメデトミジン |
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| Outline of Final Research Achievements |
We examined the role of the descending pain inhibitory system in a rat spinal nerve ligation model (Chung model) by analyzing behavioral experiments together with synaptic responses using spinal cord in vivo patch clamp method. Tramadol decreased spontaneous excitatory synaptic currents (sIPSC) and increased spontaneous inihibitory synaptic currents (sIPSC), but preparation of semi-resection of cervical cord for resection of spinal descending inihibitory pathway revealed that M1, the major metabolite of tramadol, acts at supraspinal site.
Destruction of the noradrenaline neurons at the locus coeruleus did not bring about a reverse phenomenon of allodynia at the left and the right side, therefore we were unable to confirm a mechanism that excitation of the inhibitory neurons inversely potentiated pain.
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