Schäfers Maria, Sorkin Linda
Department of Neurology, University of Duisburg-Essen, Hufelandstr. 55, 45122 Essen, Germany.
Neurosci Lett. 2008 Jun 6;437(3):188-93. doi: 10.1016/j.neulet.2008.03.052. Epub 2008 Mar 22.
Numerous studies have shown that proinflammatory cytokines induce or facilitate pain and hyperalgesia in the presence of inflammation, injury to the nervous system or cancer. Besides acting as inflammatory mediators, increasing evidence indicates that cytokines may also specifically interact with receptor and ion channels regulating neuronal excitability, synaptic plasticity and injury under both physiological and pathological conditions. Here we summarize findings on two prototypical proinflammatory cytokines, tumor-necrosis factor-alpha and interleukin-1 beta, and their effects on neuronal excitability and ion channels with special regards to pain and hyperalgesia.
大量研究表明,促炎细胞因子在存在炎症、神经系统损伤或癌症的情况下会诱导或加剧疼痛和痛觉过敏。除了作为炎症介质发挥作用外,越来越多的证据表明,细胞因子在生理和病理条件下也可能与调节神经元兴奋性、突触可塑性和损伤的受体及离子通道发生特异性相互作用。在此,我们总结了两种典型促炎细胞因子——肿瘤坏死因子-α和白细胞介素-1β的研究结果,以及它们对神经元兴奋性和离子通道的影响,特别关注疼痛和痛觉过敏方面。