Pain reduction mechanism by suppressing glial cell function in orofacial pain model

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K17044
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57050:Prosthodontics-related
• Research Institution: The University of Tokushima
• Principal Investigator: IWASA Takuma 徳島大学, 病院, 診療支援医師 (80761428)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: カルシトニン遺伝子関連ペプチド / 痛み行動 / 三叉神経節 / サテライトグリア細胞 / 炎症性サイトカイン

Outline of Final Research Achievements

Calcitonin gene-related peptide (CGRP), which is associated with pain transmission, was administered directly to the trigeminal ganglion of rats under general anesthesia and was understood to produce orofacial pain. Improvement in pain behavior was observed in rats in which the antimicrobial drug minocycline was administered to the trigeminal ganglia before CGRP administration. In addition, activation of satellite glia cell function around neurons was observed after direct administration of CGRP to the trigeminal ganglion.
In orofacial pain model in which CGRP was administered directly to the trigeminal ganglion, changes in NF-κB signaling-related mRNA expression were observed, which were observed to be close to control levels after pretreatment with minocycline.

Free Research Field

補綴系歯学

Academic Significance and Societal Importance of the Research Achievements

本研究では、口腔顔面痛モデルの三叉神経節におけるサテライトグリア細胞機能抑制による鎮痛効果メカニズムの解明と治療法の基盤形成ができたと感がられる。具体的には以下のことが解明された。(1)口腔顔面痛動物モデルにおけるサテライトグリア細胞内NF-κBシグナル伝達変化、(2)口腔顔面痛モデルの三叉神経節へのサテライトグリア細胞機能抑制薬投与による痛み行動の変化、(3)サテライトグリア細胞機能抑制によるNF-κBシグナル伝達変化などである。これにより、口腔顔面痛の新規治療法開発の足掛かりになったと考えられる。