Role of BDNF on the excitability of trigeminal ganglion neurons involved in inflammatory hyperalgesia

Research Project

Project/Area Number	24592819
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Functional basic dentistry
Research Institution	Azabu University (2014) The Nippon Dental University (2012-2013)
Principal Investigator	TAKEDA Mamoru 麻布大学, その他部局等, 教授 (20227036)
Project Period (FY)	2012-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000) Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000) Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords	三叉神経節ニューロン / BDNF / パラクリン / 炎症 / パッチクランプ法 / 免疫組織化学 / 電気泳動的投与 / 細胞外記録 / 痛覚 / 三叉神経節 / 神経栄養因子 / パッチクランプ / 蛍光標識法 / 免疫組織化学法
Outline of Final Research Achievements	Present study investigated that the functional significance of hyperalgesia to the brain-derived neurotrophic factor (BDNF) tyrosine linase B (trkB) signaling system in trigeminal ganglion (TRG) neurons projecting to the trigeminal subnuclei interpolaris/ caudalis (Vi/Vc) transition region following masseter muscle inflammation under in vivo and in vitro conditions. We found that BDNF enhances the excitability of small –diameter TRG neurons projecting onto the Vi/Vc following masseter muscle inflammation. Thus, these findings suggest that ganglionic BDNF-trk B signaling is therapeutic targets for the treatment for trigeminal inflammatory hyperalgesia