Analysis of migraine pathophysiology in an animal model using small-animal PET

使用FDG的活体PET成像和转位蛋白(TSPO，以前称为外周苯二氮卓类受体)的PET配体[^&lt；11&gt；C]PK11195，我们评估了皮质扩散性抑制(SD)后大鼠大脑中的疼痛基质和神经源性炎症过程，SD是一种用于制造偏头痛实验动物模型的刺激。结果表明，广泛用于中枢神经系统小胶质细胞成像的PK11195在单侧SD模型大鼠同侧大脑半球摄取增加，并被过量的未标记配体完全取代。此外，定量分析显示，[^&lt；11&gt；C]PK11195在同侧大脑半球的结合潜力显著增加，提示小胶质细胞激活在偏头痛病因中的病理作用。结果进一步表明，在偏头痛的几个脑区，包括同侧脑干、对侧感觉和岛叶皮质，局部脑活动显著增加，据报道，这些区域参与了偏头痛的伤害性通路。

Using in vivo PET imaging with FDG and[^<11> C] PK11195, a PET ligand for translocator protein(TSPO, previously called peripheral benzodiazepine receptor), we evaluated the pain matrix and neurogenic inflammatory process in the rat brain after generation of cortical spreading depression(SD), a stimulation used for making an experimental animal model of migraine. The results show that the uptake of[^<11> C] PK11195, which has been used extensively to image activated microglia in the central nervous system, in the unilateral SD model rats increased in the ipsilateral hemisphere, and completely displaced by excess unlabeled ligands. Moreover, a quantitative analysis showed the binding potential for[^<11> C] PK11195 to significantly increase in the ipsilateral hemisphere, suggesting a pathological role of microglia activation in migraine etiology. The results further show that the regional brain activity was significantly increased in several brain regions, including the ipsilateral brainstem, contralateral sensory, and insular cortex, which have been reported to be involved in a nociceptive pathway in migraine.