| Project/Area Number |
15K19194
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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 | Jikei University School of Medicine |
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Principal Investigator |
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| Research Collaborator |
KATO Fusao 東京慈恵会医科大学, 医学部, 教授 (20169519)
YAMAMOTO Sumii 筑波大学, 医学医療系, 講師 (50402376)
SUGIMOTO Mariko
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 情動 / 疼痛 / シナプス可塑性 / 扁桃体 / パッチクランプ記録 / モノアミン / シナプス伝達 / 神経生理学 / ノルアドレナリン / 痛み / 侵害受容性扁桃体 |
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| Outline of Final Research Achievements |
Accumulated lines of evidence indicates pain chronification is characterized by plastic changes of central nervous system. The synaptic potentiation in the amygdala in various types of pain models are reported. This study was undertaken to examine a hypothesis that noradrenergic modulation of the amygdala is one of the key mechanisms of pain chronification. For this purpose, we produced DBH-tTA-2A-cre BAC Tg rats and we injected AAV vectors for the channelrhodopsin into noradrenagic receptors. In the brain slices, we could observe light-evoked release of noradrenalin, which evoked electrophysiological responses. The involvement of endogenous noradrenalin in the central was also confirmed by evaluating the pain-associated behavior after inactivating noradrenergic neurons with DBH-saporin. Altogether, we demonstrated that endogenous adrenaline play essential role during the establishment of chronic pain.
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