Delépine L, Aubineau P
Laboratoire de Pharmacologie et de Physiopathologie Vasculaire, CNRS ESA 5017, Université Bordeaux II, France.
Exp Neurol. 1997 Oct;147(2):389-400. doi: 10.1006/exnr.1997.6614.
It has been proposed that migraine could result from a neurogenic inflammation of the dura mater. According to this theory, inflammation could be initiated by an axon reflex of nociceptive nerve fibers, but the trigger of this axon reflex remains poorly understood. Previous works have shown that parasympathetic agonists can activate mast cells and/or sensory C-fibers, inducing pain and inflammation. The aim of the present work was to determine whether the activation of intracranial parasympathetic nerve fibers could trigger an inflammatory mechanism within the rat dura mater. Activation of the intracranial parasympathetic system was achieved by electrical stimulation of the sphenopalatine ganglion (SPG). The development of a neurogenic inflammation was estimated either by microscopic examination or by quantitative measurement of plasma protein extravasation (PPE) in the dura. To determine the respective roles of the parasympathetic and sensory innervations, two groups of rats were pretreated either with atropine or with capsaicin. Stimulation of the SPG induced a PPE increase of about 200% in the stimulated side on the dura mater. Extravasated material was mainly concentrated around small blood vessels. This extravasation was significantly reduced by capsaicin pretreatment and completely abolished by atropine. Infusion of carbachol in the common carotid artery induced PPE in the ipsilateral dura comparable to that induced by electrical stimulation of the SPG. This extravasation was also blocked by atropine infusion. These data indicate for the first time that the parasympathetic nervous system can trigger a neurogenic inflammation in the dura via muscarinic cholinergic receptors. Sensory C-fibers seem to play a role in this phenomenon. With respect to the potential autonomic imbalance described in the etiology of various types of vascular headaches, such a mechanism could be important in inducing attacks.
有人提出偏头痛可能源于硬脑膜的神经源性炎症。根据这一理论，炎症可能由伤害性神经纤维的轴突反射引发，但这种轴突反射的触发因素仍知之甚少。先前的研究表明，副交感神经激动剂可激活肥大细胞和/或感觉C纤维，诱发疼痛和炎症。本研究的目的是确定颅内副交感神经纤维的激活是否能触发大鼠硬脑膜内的炎症机制。通过电刺激蝶腭神经节（SPG）实现颅内副交感神经系统的激活。通过显微镜检查或定量测量硬脑膜中的血浆蛋白外渗（PPE）来评估神经源性炎症的发展。为了确定副交感神经和感觉神经支配的各自作用，两组大鼠分别用阿托品或辣椒素进行预处理。刺激SPG可使硬脑膜刺激侧的PPE增加约200%。渗出物质主要集中在小血管周围。辣椒素预处理可显著减少这种外渗，而阿托品可完全消除这种外渗。在颈总动脉中注入卡巴胆碱可在同侧硬脑膜中诱导出与电刺激SPG相当的PPE。这种外渗也可被注入阿托品所阻断。这些数据首次表明，副交感神经系统可通过毒蕈碱胆碱能受体触发硬脑膜中的神经源性炎症。感觉C纤维似乎在这一现象中起作用。就各种类型血管性头痛病因中描述的潜在自主神经失衡而言，这样一种机制在诱发发作中可能很重要。
