摘要目的 探讨ERK1/2在偏头痛中枢发病机制中的作用.方法 6只SD大鼠随机数字表法分为:正常组(N组)、假手术组(C组)、偏头痛模型组(M组)、二甲基亚砜组(DMSO)(D组)和ERK1/2抑制剂PD-98059组(PD组),每组n=12.进行三叉神经脊束核神经元放电记录和ERK1/2磷酸化水平检测.结果 (1)放电频率变化百分比:造模后,三叉神经脊束核细胞外放电频率增加,造模后2h为造模前的(325.88±47.32)％;M放电频率(325.9±47.3)％高于N组(100.0±0.0)％和C组(107.3±16.4)％.D组放电频率(319.3±42.5)％与M组(325.9±47.3)％相比,差异无统计学意义;PD组放电频率(218.5±31.7)％低于M组(325.9±47.3)％和D组(319.3±42.5)％.(2)磷酸化水平:M组、D组ERK1/2磷酸化水平高于N组和C组;D组与M组相比,磷酸化水平无明显变化;PD组磷酸化水平低于其余四组.结论 偏头痛中枢敏感化过程中,三叉神经脊束核神经元兴奋性和ERK1/2磷酸化水平增加,ERK1/2抑制剂PD-98059能减少神经元兴奋性和ERK1/2磷酸化水平,说明ERK1/2可能参与大鼠偏头痛中枢敏感化的形成.

abstractsObjective To explore the role of ERK1/2 in the central pathogenesis of migraine.Methods Healthy adult male SD rats were randomly divided into five groups:normal group (group C),sham operation group(group C),migraine model group(group M),DMSO group (group D)and PD-98059group (PD group),with 12 rats in each group.The extracellular discharge frequency in the spinal trigeminal nucleus was recorded and ERK1/2 phosphorylation was tested.Results (1) The percentage of extracellular discharge frequency change:Two hours after treatment,the percentage of discharge frequency change was (325.9±47.32)％.The percentage of extracellula discharge frequency change in group M (325.9±47.3)％ was higher than that in group N (100.0± 0.0) ％ and group C(107.3± 16.4)％.There was no significant difference in the percentage of discharge frequency change between group D(319.3±42.5) ％ and group M (325.9±47.3) ％.The percentage of discharge frequency change in group PD(218.5±31.7)％ was lower than that in group M(325.9±47.3)％ and group D(319.3± 42.5)％.(2) ERK1/2 phosphorylation:the ERK1/2 phosphorylation in group M and group D was higher than that in group N and group C.There was no significant difference in ERK1/2 phosphorylation between group D and group M.The ERK1/2 phosphorylation in group PD was lower than the other four groups.Conclusion During the process of central sensitization to migraine,neuronal excitability and ERK1/2 phosphorylation were increased.ERK1/2 inhibitor (PD98059) reduced ERK1/2 phosphorylation and neuronal excitability.These indicated that ERK1/2 may play a role in central sensitization of migraine in rats.