Abstract：
Classical migraine patients experience aura, which is transient neurological deficits associated with cortical spreading depression (CSD), preceding headache attacks. It is not currently understood how a pathological event in cortex can affect peripheral sensory neurons. In this study, we show that cerebrospinal fluid (CSF) flows into the trigeminal ganglion, establishing nonsynaptic signaling between brain and trigeminal cells. After CSD, ~11% of the CSF proteome is altered, with up-regulation of proteins that directly activate receptors in the trigeminal ganglion. CSF collected from animals exposed to CSD activates trigeminal neurons in naïve mice in part by CSF-borne calcitonin gene-related peptide (CGRP). We identify a communication pathway between the central and peripheral nervous system that might explain the relationship between migrainous aura and headache.
摘要：
经典偏头痛患者经历先兆，与皮质扩散抑制（CSD）相关的短暂性神经功能缺损，在头痛发作之前。目前尚不清楚皮质中的病理事件如何影响外周感觉神经元。在这项研究中,我们显示脑脊液（CSF）流入三叉神经节，在大脑和三叉神经细胞之间建立非突触信号。在CSD之后，约11%的CSF蛋白质组发生改变，直接激活三叉神经节受体的蛋白质上调。从暴露于CSD的动物中收集的CSF部分地通过CSF携带的降钙素基因相关肽(CGRP)激活了原始小鼠中的三叉神经神经元。我们确定了中枢神经系统和周围神经系统之间的沟通途径，这可能解释了偏头痛先兆和头痛之间的关系。
