| Project/Area Number |
15K21604
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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 |
Basic / Social brain science
Pain science
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| Research Institution | University of Fukui |
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Principal Investigator |
Ishikawa Tatsuya 福井大学, 学術研究院医学系部門, 特命助教 (00750209)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 神経回路再編 / ニューロン・グリア連関 / 慢性疼痛 / ミラーイメージペイン / in vivo 2光子イメージング / 免疫電子顕微鏡法 / 凍結割断レプリカ法 / 一次体性感覚野 / In vivo イメージング / in vivo イメージング |
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| Outline of Final Research Achievements |
Some chronic pain patients have an abnormal pain sensation in contralateral limb to injury, which is called mirror image pain. Since synaptic remodeling in the primary somatosensory cortex (S1) has critical roles in induction of chronic pain, cortical reorganization in the S1 ipsilateral to injured limb may contribute to mirror image pain. However, contribution of cortical cells in the S1 in mirror image pain remain completely unknown.
In the present study, we found that inhibitory neuronal activities and astrocytic activities increased in the S1, while excitatory neuronal function decreased. Disinhibition of ipsilateral S1 induced by chronic application of GABAA receptor antagonist caused enhancement of neuronal activities, synaptic remodeling and chronic pain, and these are blocked by inhibition of astrocytic activities. Therefore, present results indicate that disinhibition of ipsilateral S1 to injured limb may contribute to induction of mirror image pain with synaptic remodeling.
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