Regulation of the Spontaneous Augmentation of NaV1.9 in Mouse Dorsal Root Ganglion Neurons.

Research Project

Project/Area Number	20602002
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	疼痛学
Research Institution	Hiroshima University
Principal Investigator	OGATA Nobukuni Hiroshima University, 大学院・医歯薬学総合研究科, 名誉教授 (80091255)
Project Period (FY)	2008 – 2010
Project Status	Completed (Fiscal Year 2010)
Budget Amount *help	¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000) Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000) Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2008: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Keywords	ナトリウムチャネル / 疼痛 / パッチクランプ / 一次知覚神経 / 慢性疼痛
Research Abstract	The mechanism underlying the spontaneous augmentation of NaV1.9is still unclear. We examined the effects of protein kinases A and C (PKA and PKC), on the spontaneous augmentation of NaV1.9. The spontaneous augmentation of the NaV1.9 current was significantly suppressed by activation of PKA, whereas activation of PKA did not affect the voltage dependence of inactivation for the NaV1.9 current. These results indicate that the spontaneous augmentation of NaV1.9 was regulated directly by PKA, and indirectly by PKC.