P/Q型钙离子通道与偏头痛

目的 利用硝酸甘油实验性偏头痛大鼠模型探讨P/Q型钙离子通道在偏头痛发病机制中的作用.方法 20只sD大鼠(雌雄各半)随机分为生理盐水对照组和模型组.模型组按Tassorelli Cristina法复制偏头痛大鼠模型(每周1次,连续4次),第4次造模后分别取三叉神经节及三叉颈复合体、大脑额叶组织.RT-PCR及Western-blot法测定P/Q型钙离子通道mRNA及蛋白的表达量,同时用Fluo-3/AM荧光法测定其细胞内钙离子浓度.结果 与对照组相比,模型组大鼠三叉神经节及三叉颈复合体(mRNA:0.472 36±0.049 54;蛋白:0.337 25±0.035 93)和大脑额叶组织(mRNA:0.547 45±0.044 39;蛋白:0.402 13±0.029 83)中的P/Q型钙离子通道在mRNA及蛋白水平均表达上调(t=2.6697、3.1993、3.4398、3.7661,P<0.05),同时细胞内钙离子浓度也明显高于对照组(P<0.05).结论 P/Q型钙离子通道可能通过其表达量的上调参与了偏头痛的发生发展过程.

Experimental study on the relationship between p/Q-type calcium channel and migraine

Objective To investigate the mechanism of P/Q-type calcium channel in nitroglycerin induced migraine experimental model Methods Twenty Sprague-Dawley rats ( half female and half male) were randomly divided into control group and model group. The model of migraine rats was reproduced using Tasserelli Cristina method that wassubcutaneou injection of GTN of 10 mg/kg, once a week for four weeks. After the model of migraine had been established, trigeminal ganglion and trigeminocervical complex and cortex of frontal lobe were removed and the expressions of P/Q-type calcium channel were detected by RT- PCR and Western-blot, and at the same time the concentration of intracellular Ca2+ was investigated by Fluo- 3/AM fluorometric method. Results Compared with the control group, the expression of mRNA and protein of P/Q-type calcium channel of trigeminal ganglion and trigeminocervical complex (mRNA: 0. 472 36± 0. 049 54; protein: 0. 337 25 ± 0. 035 93 ) and cortex of frontal lobe ( mRNA: 0. 547 45 ± 0. 044 39 ; protein : 0. 402 13 ± 0. 029 83) in model group all upregulated (t = 2. 6697, 3. 1993, 3. 4398 and 3. 7661, all P <0. 05), at the same time the concentration of intracellular Ca2+ in model group increased (211 182 ± 12 973 vs 135 243 ± 18 105 in trigeminal ganglion and trigeminocervical complex; 186 511 ± 18 297 vs 143 289±25 175 in cortex of frontal lobe. t =10.7819 and 4. 3917, beth P<0.05). Conclusions P/Q- type calcium channel may play a role in the pathogenesis of migraine via its upregulated expression.