Role of CCL2/CCL2 receptor signaling within trigeminal ganglia on the inflammatory pain
| Project/Area Number |
15K11058
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Azabu University |
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Principal Investigator |
Takeda Mamoru 麻布大学, 生命・環境科学部, 教授 (20227036)
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 三叉神経節 / ケモカイン / 炎症 / 痛覚過敏 / パッチクランプ / 免疫組織化学 / 逃避反射 / ＣＣＬ２ / CCL2 / CCR2 |
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| Outline of Final Research Achievements |
This study investigated the functional significance of hyperalgesia in the CCL2/CCL2 receptor signaling system in trigeminal ganglion (TG) neurons following inflammation, using behavioral, immunohistochemical and electrophysiological analysis.The present study provides evidence that CCL2 enhances the excitability of small-diameter TG neurons following facial skin inflammation via the upregulation of CCL2/CCL2 receptor signaling. These findings suggest that ganglionic CCL2/CCL2 receptor signaling is a therapeutic molecular target for the treatment of trigeminal inflammatory hyperalgesia.
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Report
(4 results)
Research Products
(1 results)
