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痛觉敏感化与蛋白激酶
外周神经受损或外周组织受炎症刺激时,常出现痛觉过敏(hyperalyesia,Ha)、痛觉超敏( allodynia,Al) 和自发痛(spontaneous pain,Sp) 等反应性增强或敏感化表现.痛觉过敏是对伤害性刺激产生过强的反应;痛觉超敏指对非伤害性刺激产生伤害性反应;自发痛则为在没有可见刺激条件下出现的疼痛.许多研究表明,痛觉过敏等反应性增强过程可能与中枢敏感化有关,各种致痛性物质、神经递质及其引起的胞内第二信使的变化在中枢敏感化的形成过程中发挥了重要的作用[1] .
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加巴喷丁对大鼠偏头痛中枢敏感化及脑脊液氨基酸含量的影响
目的:探讨加巴喷丁对大鼠偏头痛中枢敏感化及脑脊液氨基酸含量的影响.方法:选取200～250 g雄性SD大鼠共60只；随机均分为正常组(N组)、假手术组(C组)、偏头痛模型组(M组)、生理盐水组(NS组)和加巴喷丁组(G组)；每组12只.进行三叉神经脊束核神经元放电记录和脑脊液氨基酸含量检测.结果: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321.81±47.43％;C组和N组放电频率相比,差异无显著性(P＞0.05);M组与NS组放电频率相比,差异无显著性(P＞0.05)；G组与M组相比,放电频率显著性下降(P＜0.01).与N组相比,M、G组兴奋性氨基酸显著性增加(P＜0.01);G组与M组相比,兴奋性氨基酸显著性减少(P＜0.01)；M组、G组与N组相比,抑制性氨基酸显著性减少(P＜0.0l)；G组和M组相比,氨基酸水平无显著性差异(P＞0.05).结论:加巴喷丁可能通过兴奋性氨基酸信号通路抑制偏头痛中枢敏感化.
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曲马多对急性心肌缺血大鼠丘脑束旁核5-HT1A受体mRNA表达的影响
心肌缺血时通过中枢和外周痛觉敏感化机制,心脏交感传入冲动增加,从而有可能诱发心绞痛.但由心肌缺血引发的心绞痛(症状)和急性心肌梗死(损伤)的程度往往不相平行[1].丘脑束旁核(parafascicular nucleus,Pf)是内脏痛觉感受、调制和整合的重要中枢,Pf内含有丰富的5-HT能神经末梢及其受体.
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丝裂原活化的蛋白激酶激活通路与病理性痛痛觉敏感化
Pathological pain or clinical pain is caused by tissue and nerve injuries, and is usually chronic and mainly divided into inflammatory pain and neuropathic pain. Pathological pain is typically characterized by hyperalgesia (increased responsiveness to noxious stimuli) and allodynia (painful responses to normally innocuous stimuli). The mitogen-activated proteins kinases (MAPKs) are a family of evolutionally conserved molecules that play a critical role in cell signaling, consisting of extracellular signal regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), which play an important role in neural plasticity of pathological pain. Inhibition of MAPKs alleviates inflammatory pain and neuropathic pain in different animal models. It is very important to study the inhibition of MAPKs as a therapeutic approach to treat pathological pain.
关键词： 有丝分裂素激活蛋白激酶类 病理性痛 痛觉敏感化
