MODULATION OF FACIAL AND DENTAL PAIN TRANSMISSION BY ENKEPHALIN IN TRIGEMINAL GANGLION

三叉神经节中脑啡肽对面部和牙齿疼痛传递的调节

• 批准号: 03670866
• 负责人: MAEDA Sadaaki
• 金额: $ 1.28万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1991
• 资助国家: 日本
• 起止时间: 1991 至 1992
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-03670866/
• 关键词: Trigeminal ganglion; Opiate receptor; Calcium channel; Enkephalin; Pain transmission

Our previous report showed that leucine-enkephalin immunoreactive nerve fibers and cell bodies occurred in trigeminal ganglion of the guinea pig, suggesting the possibility that leucine-enkephalin can modulate pain transmission in trigeminal ganglion. In this research, we characterized opioid receptors and voltage-dependent calcium channels in trigeminal ganglion of giunea pig.1) The values of Kd and Bmax of ^3H-DPDPE (selective ligand for delta - type opiate receptors) and ^3H-DAMGO (selective ligand for mu - type opiate receptors) were 4.4nM, 29.1 fmol/mg protein and 0.7 nM, 7.2 fmol/mg protein, respectively.2) The values of Kd and Bmax of ^3H-PN200-110 (L-type calcium channel antagonist) and ^<125>I-omega- conotoxin (N-type calcium channel antagonist) were 48.2 pM, 18.5 fmol/mg protein and 50.1 pM, 29.5 fmol/mg protein, respectively.3) Acute administration of morphine did not affect both ^3H-PN200-110 and ^<125>I-omega-conotoxin binding. The chronic administration increased the binding of ^<125>I-omega-conotoxin.4) Using laser scanning fluorescence microscope, we found that leucine-enkephalin-immunorective fibers surrounded some nonimmunoreactive ganglionic cells.These results suggest that leucine-enkephalin may modulate the function of the primary afferent neuron through calcium dynamics in guinea pig trigeminal ganglion.

我们之前的报道显示，在豚鼠三叉神经节中出现了亮氨酸-脑啡肽免疫反应的神经纤维和细胞体，提示亮氨酸-脑啡肽可能调节三叉神经节的疼痛传递。在本研究中，我们对豚鼠三叉神经节中阿片受体和电压依赖性钙通道进行了表征。1) δ型阿片受体选择性配体^3H-DPDPE和μ型阿片受体选择性配体^3H-DAMGO的Kd和Bmax分别为4.4nM、29.1 fmol/mg蛋白和0.7 nM、7.2 fmol/mg蛋白。2) ^3H-PN200-110 （l型钙通道拮抗剂）和^<125>I-omega- conotoxin （n型钙通道拮抗剂）的Kd和Bmax分别为48.2 pM、18.5 fmol/mg蛋白和50.1 pM、29.5 fmol/mg蛋白。3)急性给药吗啡不影响^3H-PN200-110和^<125> i -omega- concontoxin结合。慢性给药增加了^<125> i -omega- concontoxin的结合。4)在激光扫描荧光显微镜下，我们发现亮氨酸-脑啡肽免疫纤维包围了一些非免疫反应的神经节细胞。提示亮氨酸-脑啡肽可能通过钙动力学调节豚鼠三叉神经节初级传入神经元的功能。