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.

本研究的目的是研究三叉神经节中的神经胶质交叉说话是否有助于调节周围感染期间伤害性三叉神经元神经元的神经元令人兴奋。将完整的新生（CFA）注入大鼠面部皮肤以产生感染。在发炎大鼠中施加到晶须垫上的机械刺激的阈值明显低于对照组的阈值。注射CFA两天后，在同一细胞中，通过神经胶质原纤维酸性蛋白（GFAP）/IL-1β免疫反应率包围的TRG神经元的平均百分比百分比。荧光标记确定了炎症部位。在发炎的大鼠中，FG标记的IL-1受体I型（IL-1RI）小TRG神经元的数量明显大于对照组。在标有小TRG神经元的FG中，在发炎的大鼠Aσ-不感染的TRG神经元中，IL-1β诱导的peLARISATION在五边形麻醉大鼠中记录了对晶须垫的电刺激的响应。具有赞助器发射的Aσ-TRG神经元的数量及其发炎大鼠的发射率明显大于对照大鼠。 Aσ-TRG神经元赞助子活性的发射速率目前通过局部离子噬术在发炎的大鼠中局部离子噬菌体应用I受体I型拮抗剂（IL-1RA）降低。发炎大鼠的伤害性-TRG神经元的机械阈值明显低于对照大鼠的机械阈值，但在对照大鼠和IL-1RA施用后，对照大鼠和发炎的大鼠之间没有显着差异。这些结果表明，在发炎的调制下，伤害感受性Aσ-TRG神经元通过三叉神经节内的IL-1β旁分泌作用支配面部皮肤。这样的IL-1β释放对于确定三叉神经炎症性痛觉过敏可能很重要。