Cortical Spreading Depression, Meningeal Inflammation and Trigeminal Nociception

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.