Wei Xiaomei, Melemedjian Ohannes K, Ahn David Dong-Uk, Weinstein Nicole, Dussor Gregory
Department of Pharmacology, University of Arizona School of Medicine, Tucson, AZ, USA.
Pain. 2014 Jul;155(7):1238-1244. doi: 10.1016/j.pain.2014.03.013. Epub 2014 Mar 20.
Nociceptive signaling from the meninges is proposed to contribute to many forms of headache. However, the events within the meninges that drive afferent activity are not clear. Meningeal fibroblasts are traditionally thought to produce extracellular proteins that constitute the meninges but not to contribute to headache. The purpose of these studies was to determine whether dural fibroblasts release factors that activate/sensitize dural afferents and produce headache-like behavior in rats. Dura mater was removed from male rats and dural fibroblasts were cultured. Fibroblast cultures were stimulated with vehicle or lipopolysaccharide (LPS), washed, and conditioned media was collected. Fibroblast media conditioned with vehicle or LPS was applied to retrogradely labeled rat dural trigeminal ganglion neurons in vitro. Patch-clamp electrophysiology was performed to determine whether conditioned media activated/sensitized dural afferents. A preclinical behavioral model was used where conditioned media was applied directly to the rat dura to determine the presence of cutaneous facial and hind-paw allodynia. Conditioned media was also tested for interleukin-6 (IL-6) content using an enzyme-linked immunosorbent assay. Application of LPS-conditioned fibroblast media to dural afferents produced a significant increase in action potential firing as well as cutaneous facial and hind-paw allodynia when this media was applied to the dura. Finally, stimulation of cultured fibroblasts with LPS increased IL-6 levels in the media. These findings demonstrate that fibroblasts stimulated with LPS release factors capable of activating/sensitizing dural afferents. Further, they suggest that fibroblasts play a potential role in the pathophysiology of headache.
脑膜的伤害性信号传导被认为与多种形式的头痛有关。然而,驱动传入活动的脑膜内事件尚不清楚。传统上认为脑膜成纤维细胞产生构成脑膜的细胞外蛋白质,但与头痛无关。这些研究的目的是确定硬脑膜成纤维细胞是否释放能够激活/致敏硬脑膜传入神经并在大鼠中产生类似头痛行为的因子。从雄性大鼠身上取出硬脑膜并培养硬脑膜成纤维细胞。用载体或脂多糖(LPS)刺激成纤维细胞培养物,洗涤后收集条件培养基。将用载体或LPS处理过的成纤维细胞培养基应用于体外逆行标记的大鼠硬脑膜三叉神经节神经元。进行膜片钳电生理学以确定条件培养基是否激活/致敏硬脑膜传入神经。使用临床前行为模型,将条件培养基直接应用于大鼠硬脑膜,以确定是否存在面部皮肤和后爪痛觉过敏。还使用酶联免疫吸附测定法检测条件培养基中的白细胞介素-6(IL-6)含量。将LPS处理的成纤维细胞培养基应用于硬脑膜传入神经时,动作电位发放显著增加,并且当将该培养基应用于硬脑膜时会出现面部皮肤和后爪痛觉过敏。最后,用LPS刺激培养的成纤维细胞会增加培养基中的IL-6水平。这些发现表明,用LPS刺激的成纤维细胞释放能够激活/致敏硬脑膜传入神经的因子。此外,它们表明成纤维细胞在头痛的病理生理学中可能发挥作用。