Sensitization of trigeminal nervous system by infraorbital nerve injury exacerbates the pathophysiology of migraine

我们采用离子松扎法建立眶下神经慢性收缩损伤（ION- cci）大鼠模型作为慢性口面部疼痛模型（神经性疼痛模型）。ION-CCI后3周，采用10mM辣椒素刺激大鼠硬脑膜（偏头痛模型之一），免疫组化染色法检测三叉神经脊髓尾侧亚核磷酸化细胞外信号调节激酶（pERK）的表达。结果表明，与辣椒素刺激组相比，离子- cci +辣椒素刺激组的perk -免疫反应神经元在尾侧超过1440 μm之间显著增加。综上所述，离子- cci对三叉神经第二支的致敏作用影响辣椒素对三叉神经第一支的激活，提示慢性口面部疼痛可能加重偏头痛的病理生理。

We established the chronic constriction injury of the infraorbital nerve (ION-CCI) rat model as a chronic orofacial pain model (neuropathic pain model) by ION loose ligation. At 3 weeks after ION-CCI, the dura was stimulated by 10mM capsaicin, which was the one of the migraine models, followed by checking the expression of the phosphorylated extracellular signal-regulated kinase (pERK) at the trigeminal spinal subnucleus caudalis by immunohistochemical staining method. It showed that the pERK-immunoreactive neurons statistically increased between ovex and 1440 μm caudally in ION-CCI + capisaisin stimulating group compared to capsaicin stimulating group. Taken together, the sensitization of 2nd branch of trigeminal nerve by ION-CCI affected the activation of 1stbranch of trigeminal nerve by capsaicin, suggesting that chronic orofacial pain may exacerbates the pathophysiology of migraine.