Messlinger K, Hanesch U, Kurosawa M, Pawlak M, Schmidt R F
Department of Physiology, University of Würzburg, Germany.
Can J Physiol Pharmacol. 1995 Jul;73(7):1020-4. doi: 10.1139/y95-143.
The parietal dura mater encephali of the rat was shown by immunohistochemistry to be densely innervated by calcitonin gene related peptide (CGRP) immunoreactive nerve fibers spreading around the medial meningeal artery and its branches. Electrical stimulation of the dural surface (10-20 V, 5-10 Hz, 10-30 min) caused a depletion of CGRP-immunopositive fibers, suggesting a release of CGRP. The dural blood flow around branches of the medial meningeal artery was also monitored with a laser Doppler flowmeter. Short periods (30 s) of electrical stimulation with parameters that presumably released CGRP form nerve fibers caused a repeatable and constant increase of the blood flow for 1-2 min. This evoked increase could dose dependently be inhibited by topical application of the CGRP antagonist hCGRP8-37. Accordingly, administration of hCGRP increased the basal blood flow. We conclude that stimulation of trigeminal afferents innervating the dura mater releases CGRP from peptidergic afferent terminals, thereby causing vasodilatation and increasing the meningeal blood flow, an important element of neurogenic inflammation.
免疫组织化学显示，大鼠脑顶硬脑膜有密集的降钙素基因相关肽（CGRP）免疫反应性神经纤维支配，这些神经纤维分布在脑膜中动脉及其分支周围。对硬脑膜表面进行电刺激（10 - 20V，5 - 10Hz，10 - 30分钟）会导致CGRP免疫阳性纤维减少，提示CGRP释放。还用激光多普勒血流仪监测了脑膜中动脉分支周围的硬脑膜血流。用可能从神经纤维释放CGRP的参数进行短时间（30秒）电刺激，会使血流在1 - 2分钟内出现可重复且持续的增加。这种诱发的血流增加可被局部应用CGRP拮抗剂hCGRP8 - 37剂量依赖性地抑制。相应地，给予hCGRP会增加基础血流。我们得出结论，刺激支配硬脑膜的三叉神经传入纤维会从肽能传入终末释放CGRP，从而引起血管舒张并增加脑膜血流，这是神经源性炎症的一个重要因素。
