| Project/Area Number |
24791558
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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 |
Orthopaedic surgery
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| Research Institution | Kansai University of Health Sciences |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 脊髄損傷後疼痛 / in vivo パッチクランプ法 / ミクログリア / 脊髄損傷 / spinal cord injury / 神経障害性疼痛 / 神経可塑性 / 中枢性感作 / シグナル伝達 / Spinal cord injury / パッチクランプ法 / in vivo パッチクランプ / 慢性疼痛 |
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| Research Abstract |
We investigated the mechanisms of neuropathic pain after spinal cord injury (SCI) by in vivo patch-clamp methods. We analyzed the spontaneous excitatory postsynaptic currents (sEPSCs) of the dorsal horn neurons in below injury level. The average frequency of the sEPSCs in the SCI model rats was significantly larger than that in the sham model rats. This result suggests that the spinal excitatory synaptic plasticity was produced at the dorsal horn neurons in below injury level of the SCI pain model. Next, we examined the effect of the microglial activity inhibitor, Minocycline onto the excitatory synaptic transmission of SCI model rats. Contrary to our expectations, the application of Minocycline did not reduce the frequency of sEPSCs in the SCI model rats.
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