中文摘要：

目的通过炎性介质（IM）和降钙素基因相关肽（CGRP）诱发偏头痛反复发作，运用全细胞膜片钳的方法观察大鼠三叉神经节小直径神经元电压门控性钾电流的变化。方法雄性SD大鼠15只，分为空白组（不做任何干预）、生理盐水组和IM＋CGRP组（大鼠硬脑膜上埋置PE-10管，连续7d给予等量生理盐水和IM＋CGRP）。用VonFrey毛测定大鼠眶周皮肤机械痛阂。在急性分离的三叉神经节小直径神经元上，通过全细胞膜片钳方法记录延迟外向钾电流（Ik）和瞬时外向钾电流（IA）的变化。结果给药7d后，IM＋CGRP组大鼠的眶周机械痛阈明显降低，生理盐水组眶周机械痛阈无明显改变。生理盐水组三叉神经节神经元膜上总钾电流、Ik、IA与空白组比较无明显差异；IM＋CGRP组三叉神经节神经元膜上总钾电流、Ik、IA与空白组和生理盐水组比较明显减小。结论IM和CGRP诱发偏头痛反复发作模型大鼠的三叉神经节中急性分离神经元的Ik和IA明显降低，提示电压门控性钾通道可能参与了外周机械痛阂的降低。

英文摘要：

Aim To observe the changes of the voltage-gated potassium currents in small trigeminal ganglion neurons underlying inflammatory mediator （IM） and calcitonin gene-related peptide（CGRP） induced by dural afferent sensitization. Methods 15 SD male rats were divided into three groups. Normal group was set up. Physiological saline group were infused physiological saline through PE-10 tubing on the dura. IM and CGRP were applied through PE-10 tubing on the dura in IM＋CGRP group. Infusion was repeated once a day for seven days. Von Frey test and whole-cell patch clamp recording were used. Results After 7 days, the periorbital pressure threshold in IM＋CGRP rats decreased significantly after being applied IM and CGRP on the dura. The periorbital pressure threshold in physiological saline rats had no difference compared with the normal rats. Delayed rectifier potassium currents （10 in IM＋CGRP group trigeminal ganglion neurons decreased significantly compared with the normal group. Transient outward potassium currents （In） also reduced significantlycompared with those in the normal group and physiological saline group. Conclusion The study showed that the decrease of IA and IK might contribute to the decrease in periorbital mechanical pain threshold and peripheral hyperalgesia.