| Project/Area Number |
15K21410
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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 |
Social dentistry
Pain science
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| Research Institution | Nihon University |
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Principal Investigator |
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 神経障害性疼痛 / 神経‐グリア機能連関 / 慢性ストレス / カルシトニン遺伝子関連ペプチド / リン酸化細胞外シグナル調節キナーゼ / ATP受容体 / プロジェクションニューロン / 三叉神経 / サテライトグリア / 末梢感作 / 中枢感作 / エピジェネティック制御 / 三叉神経節 / サテライトグリア細胞 |
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| Outline of Final Research Achievements |
The aim of this study was to elucidate the peripheral and central nervous mechanisms underlying neuropathic tongue pain and chronic stress. The present findings suggest that calcitonin gene-related peptide (CGRP) released from trigeminal ganglion (TG) neurons activates satellite glial cells (SGCs) through extracellular signal-regulated kinase phosphorylation, resulting in the enhancement of TG neuronal excitability under tongue neuropathic pain. The phenotypic switching of large TG neurons expressing CGRP may account for persistent tongue pain. The functional interaction between SGCs activation via P2Y12R and TG neurons expressing CGRP is a significant contributor to cause neuropathic tongue pain. Our data also suggest that the change in TRPV1 expression via an alteration of epigenetic regulation under the chronic stress or neuropathic pain may cause central sensitization of trigeminal spinal subnucleus caudalis neurons resulting in the exacerbation of tongue neuropathic pain.
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