偏头痛模型大鼠三叉神经脊束核磷酸化ERK1/2水平变化

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.

Changes of the level of phosphorelated ERK1/2 in the spinal trigeminal nucleus of migraine model rats

Objective 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.