| Project/Area Number |
15K19195
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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 |
Pain science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
NAGUMO Yasuyuki 筑波大学, 国際統合睡眠医科学研究機構, 助教 (00459661)
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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 |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 脳・神経 / 体性感覚視床 / 末梢神経損傷 / GABA シナプス / 内側毛帯線維 / 神経回路再改編 / 痛覚過敏反応 / 体性感覚視床神経回路 / 回路改編 / GABAシナプス / VPM細胞 / 痛覚過敏 |
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| Outline of Final Research Achievements |
Peripheral nerve injury induces functional and structural remodeling of neural circuits along the somatosensory pathway, and this remodeling is thought to underlie ectopic abnormal sensation. However, molecular mechanism of injury-induced remodeling is largely unknown. We have previously reported the transection of the infraorbital nerve remodels excitatory lemniscal fiber synapses to somatosensory thalamic neurons. Here we found that extrasynaptic GABA-A receptor (GABA-A R)-mediated currents in the thalamic neuron were potentiated soon after the transection before the remodeling. Pharmacological potentiation of thalamic extrasynaptic GABA-A R currents in intact mice induced the similar abnormal remodeling. Notably, conditional knockout of extrasynaptic GABA-A Rs in the thalamus rescued the injury-induced remodeling as well as the ectopic mechanical hypersensitivity. Together, our results uncover a molecular basis of neural remodeling in the thalamus after peripheral nerve injury.
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