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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.

本研究的目的是探讨三叉神经节的神经元-胶质交叉对话是否有助于外周炎症期间三叉神经节痛觉神经元兴奋性的调节。将完全弗里德佐剂（CFA）注入大鼠面部皮肤，引起炎症反应。炎症大鼠须垫机械刺激的逃逸阈值明显低于对照组。注射CFA 2 d后，相同细胞中被胶质纤维酸性蛋白(GFAP)/ il -1β免疫反应环绕的TRG神经元的平均百分比共表达。氟金标签确定了炎症部位。炎症大鼠中fg标记的IL-1受体I型（IL-1RI）小TRG神经元数量显著高于对照组。在FG标记的TRG小神经元中，炎症大鼠IL-1β诱导去极化的大小比对照组大。实验记录了戊巴比妥麻醉大鼠须垫电刺激下的一个σ-痛觉性TRG神经元的反应。炎症大鼠自发性放电的Aσ-TRG神经元数量和放电速率均显著高于对照组。局部离子化应用IL-1ra后，炎症大鼠Aσ-TRG神经元自发活动的放电率呈电流依赖性降低。炎症大鼠损伤性trg神经元的机械阈值显著低于对照组，但IL-1ra离子电泳后，炎症大鼠与对照组之间无显著差异。这些结果表明，炎症作用下，三叉神经节内IL-1β的旁分泌作用可调节支配面部皮肤的a - σ- trg神经元的兴奋性。这种IL-1β释放在确定三叉神经节炎性痛觉过敏中可能是重要的。