2016 Fiscal Year Final Research Report
New mechanisms of neuropathic pain after spinal cord injury
| Project/Area Number |
15K15205
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pain science
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Keywords | 神経傷害性疼痛 / 脊髄損傷 / Ca チャネル / アロディニア |
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| Outline of Final Research Achievements |
We found the following findings using a rat model of thoracic spinal cord injury to examine the role of Ca channel subunitα2δ1 on the mechanical allodynia in the plantar surface. 1.Rat model of spinal cord injury at Th10 level showed the significant decrease in the threshold of mechanical stimuli to the plantar surface, which continued from 14-28d after spinal cord injury. 2.At 28d after SCI, theα2δ1 immunoreactivity in the lumbar spinal cord increased significantly. 3.α2δ1 mRNA in lumbar DRG showed no change after SCI, however in situ hybridization histochemistry revealed the increase in α2δ1 mRNA in superficial laminae of lumbar dorsal horn. 4. Oral administration of pregabalin (α2δ1 ligand) significantly reversed the decrease in the threshold of mechanical stimuli and also the upregulation ofα2δ1 protein in lumbar dorsal horn. The significance of the changes inα2δ1 in lumbar dorsal horn after thoracic SCI has been discussed.
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| Free Research Field |
神経解剖学
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