Cortical spreading depression, meningeal inflammation and trigeminal nociception
Cortical spreading depression, meningeal inflammation and trigeminal nociception
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皮质扩散抑制、脑膜炎症和三叉神经伤害感受
DOI：
10.1097/01.wnr.0000134989.89428.3b
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发表时间：
2004
期刊：
影响因子：
1.7
通讯作者：
A. Srikiatkhachorn
中科院分区：
文献类型：
--
作者：
S. Maneesri;Juntima Patamanont;S. Patumraj;A. Srikiatkhachorn
本研究探讨血管周围炎症是否在皮质扩散性抑制(CSD)诱导的三叉神经血管伤害性反应过程中是必要的。大鼠顶面应用氯化钾诱导CSD。用活体荧光摄像显微镜、激光多普勒血流仪和电子显微镜观察大脑皮层微循环。以Fos免疫反应为指标测定三叉神经伤害性反应。我们发现KCl2的应用引起周期性皮质充血和软脑膜微血管扩张。未见白细胞-血管内皮细胞黏附增加或大分子渗出。超微结构检查显示内皮细胞吞噬增加，但紧密连接保持完好。尽管没有强烈的血管周围炎症，我们观察到三叉神经尾侧核Fos免疫反应显著增加。这些结果表明，在CSD诱发的三叉神经血管伤害性反应过程中，血管周围炎症不是必需的。
This study investigated whether perivascular inflammation is necessary in the process of cortical spreading depression (CSD)-induced trigeminovascular nociception. CSD was induced by application of potassium chloride on rat parietal surface. Cortical microcirculation was studied using intravital fluorescent videomicroscopy, laser Doppler flowmetry and electron microscopy. Trigeminal nociception was determined using Fos immunoreactivity as the indicator. We found that KCl application caused cyclic cortical hyperaemia and pial microvascular dilation. Neither increased leukocyte-endothelial adhesion nor extravasation of macromolecule was demonstrated. Ultrastructural study revealed increased endothelial pinocytosis but tight junction remained intact. Despite no intense perivascular inflammation, we observed significantly increased Fos-immunoreactivity in trigeminal nucleus caudalis. These results suggest that perivascular inflammation is not necessary in the process of CSD-evoked trigeminovascular nociception.