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Role of neuron-glial cross talk in the trigeminal ganglia to hyperalgesia

三叉神经节中神经元-胶质细胞串扰对痛觉过敏的作用

基本信息

批准号：
17591953
负责人：
TAKEDA Mamoru
金额：
$ 2.27万
依托单位：
The Nippon Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2007
项目状态：
已结题

项目摘要

The aim of the present study was to investigate whether neuron-glial cross talk in the trigeminal ganglia contribute to modulation of neuronal excitability of nociceptive trigeminal ganglion neurons during peripheral inflammation. Complete freund's adjuvant (CFA) was injected into rat facial skin to produce inflammation. The threshold for escape from mechanical stimulation applied to the whisker pad in inflamed rats was significantly lower than that in control. Two days after CFA injection, the mean percentage of TRG neurons encircled by glial fibrillary acidic protein (GFAP)/IL-1βimmunoreactivities were coexpressed in the same cells. Fluorogold labeling identified the site of inflammation. The number of FG-labeled IL-1 receptor type I (IL-1RI) small TRG neurons in inflamed rats was significantly greater than thai in control. In the FG labeled small TRG neurons, the size of IL-1β induced-depolarization in inflamed rats was larger than in control. Aσ-nociceptive TRG neurons responding to electrical stimulation of the whisker pad was recorded in pentobarbital-anesthetized rats. The number of Aσ-TRG neurons with spontaneous firings and their firing rate in inflamed rats were significantly larger than in control rats. The firing rates of the Aσ-TRG neuronal spontaneous activity were current-dependently decreased by local iontophoretic application of an interleukin I receptor type I antagonist (IL-1ra) in inflamed rats. The mechanical threshold of nociceptive-TRG neurons in inflamed rats was significantly lower than that in control rats, but was not significantly different between control rats and inflamed rats after iontophoretic application of an IL-1ra. These results suggest that under inflammation modulates the excitability of nociceptive Aσ-TRG neurons innervating the facial skin via IL-1β paracrine action within trigeminal ganglia. Such an IL-1β release could be important in determining trigeminal inflammatory hyperalgesia.

本研究的目的是调查三叉神经节中的神经元-胶质细胞串扰是否有助于调节外周炎症期间伤害性三叉神经节神经元的神经元兴奋性。将完全弗氏佐剂（CFA）注射到大鼠面部皮肤中以产生炎症。发炎大鼠的胡须垫逃避机械刺激的阈值显着低于对照组。注射 CFA 两天后，被胶质纤维酸性蛋白 (GFAP)/IL-1β 免疫反应性包围的 TRG 神经元的平均百分比在相同细胞中共表达。荧光金标记确定了炎症部位。发炎大鼠中 FG 标记的 I 型 IL-1 受体 (IL-1RI) 小 TRG 神经元的数量明显多于对照组。在 FG 标记的小 TRG 神经元中，炎症大鼠中 IL-1β 诱导的去极化的大小比对照组大。在戊巴比妥麻醉的大鼠中记录了对触须垫电刺激做出反应的 Aσ 伤害性 TRG 神经元。发炎大鼠中自发放电的 Aσ-TRG 神经元数量及其放电率显着高于对照大鼠。在发炎大鼠中局部使用白细胞介素 I 受体 I 型拮抗剂 (IL-1ra) 进行离子电渗疗法后，Aσ-TRG 神经元自发活动的放电率呈电流依赖性降低。炎症大鼠中伤害性TRG神经元的机械阈值显着低于对照大鼠，但在离子导入IL-1ra后对照大鼠和炎症大鼠之间没有显着差异。这些结果表明，炎症状态下通过三叉神经节内的 IL-1β 旁分泌作用调节伤害性 Aσ-TRG 神经元的兴奋性，这些神经元支配面部皮肤。这种 IL-1β 的释放对于确定三叉神经炎症性痛觉过敏可能很重要。