偏头痛模型大鼠三叉神经脊束核和三叉神经节中PACAP及CGRP表达的变化

CHANGES IN THE EXPRESSION OF PACAP AND CGRP IN THE TRIGEMINAL NUCLEUS CAUDALIS AND TRIGEMINAL GANGLION IN A RAT MODEL OF MIGRAINE

目的测定偏头痛模型大鼠三叉神经脊束核(TNC)和三叉神经节(TG)内垂体腺苷酸环化酶激活肽(PACAP)、降钙素基因相关肽(CGRP)含量,从而探讨其参与偏头痛发病和慢性化过程的机制。方法 SD大鼠32只,随机分为4组,分别为炎症汤连续刺激7d组(IS-7d组)、14d组(IS-14d组)、21d组(IS-21d组)以及生理盐水连续刺激21d组(NS-21d组)。连续21d给予大鼠上矢状窦旁硬脑膜炎症汤化学刺激构建偏头痛模型,测定大鼠疼痛阈值,应用免疫组化方法测定大鼠TNC和TG内PACAP、CGRP的表达水平。结果炎症汤反复化学刺激大鼠可导致偏头痛慢性化和痛觉敏化的现象。PACAP在TG的阳性细胞数先增多后减少,在TNC中逐渐减少。CGRP在TNC和TG的阳性细胞数缓慢减少。结论 PACAP与CGRP在偏头痛的发病机制中存在相互影响,对于二者的共存释放关系以及受体拮抗剂的研究可以为未来偏头痛治疗药物的开发提供依据。

Objective To investigate the expression of pituitary adenylate cyclase-activating polypeptide(PACAP)and calcitonin gene-relatedpeptide(CGRP)inthe trigemiinal nucleus caudalis(TNC)and trigemiinal ganglion(TG)in a ratmodel of migraine,and torevealthe roles of PACAP and CGRP in the pathogenesis and chronicity of migraine.Atotalof32 Sprague-DawLey ratswere randomly assigned to be stimulated with in flammatory soup(IS)for 7 consecutive days(IS-7d group),14 consecutive days(IS-14d group),or 21 consecutive days(IS-21dgroup)or stimulated with normalsaline for 21 consecutive days(NS-21d group).The ratswere given IS at the para-superior sagittal sinus dura mater for 21 consecutive days to establish a mii-grainemodel.The pain threshold of rats was determined.The expression of PACAP and CGRP in the TNC and TG was determined by immunohis to chemitry.Result Repeated chemiical stimulation with IS led to chronic miigraine and pain sensitization in these rats.The numiber of PACAP-positive cells in the TG first increased and then decreased,while it decreased gradually in the TNC.The numibers of C'GRP-positive cells in the TNC and TG decreased slowly.PACAP and CGRP interact with each other in thepathogenesisofmiigraine.Thestudy of the coexistence and release relationship between them and receptor antagonists can provide a basis for future development of migraine drugs.