2019 Fiscal Year Final Research Report
Elucidation of the mechanism of pain caused by dental pulp inflammation: mechanical sensitivity of dental pulp inflammation-specific C neurons
| Project/Area Number |
19K21373
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| Project/Area Number (Other) |
18H06284 (2018)
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Multi-year Fund (2019)
Single-year Grants (2018) |
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| Review Section |
0907:Oral science and related fields
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| Research Institution | Tokyo Dental College |
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Principal Investigator |
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| Project Period (FY) |
2018-08-24 – 2020-03-31
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| Keywords | 歯髄炎 / 歯髄内圧上昇 / 機械刺激受容器 |
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| Outline of Final Research Achievements |
TG neurons were classified based on the shape and current duration of the voltage-dependent ionic currents; neurons showing long current duration with bump (bump(+)-TG neuron) or short current duration without it (bump(-)-TG neuron). The mechanical stimulation evoked-currents in these neurons were composed by two phases; a transient current (first component) with fast activation and inactivation kinetics and lasting currents (second component) with slow activation and inactivation. Repetitive stimuli showed no desensitizing effects on the mechanical stimulation-induced currents. Gd3+ (1 μM) significantly inhibited the mechanical stimulation induced-current amplitudes in a part of the bump(-)-TG neurons, and a part of bump(+)-TG neurons. This inhibition was not seen in some neurons, however.
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| Free Research Field |
口腔科学およびその関連分野/口腔生理
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| Academic Significance and Societal Importance of the Research Achievements |
三叉神経節ニューロンの機械感受性イオンチャネルを電気生理学的・分子生物学的に解析した報告はない. 本研究は, 機械受容の点から歯髄痛覚発生メカニズムを解明するという点で学術的独自性がある. 直接機械刺激を加え機械感受性イオンチャネル特性を解析する報告も極めて限られ技術的難易度も高い. 歯髄の痛みの発生メカニズムを解明することで, 将来的な疼痛制御薬剤の開発につながると考えられその学術的意義は非常に高い.
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