Grace Peter M, Gaudet Andrew D, Staikopoulos Vasiliki, Maier Steven F, Hutchinson Mark R, Salvemini Daniela, Watkins Linda R
Department of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado, Boulder, CO, USA; Current address: Department of Critical Care Research, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Department of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado, Boulder, CO, USA.
Trends Neurosci. 2016 Dec;39(12):862-879. doi: 10.1016/j.tins.2016.10.003. Epub 2016 Nov 12.
Tissue injury can initiate bidirectional signaling between neurons, glia, and immune cells that creates and amplifies pain. While the ability for neurotransmitters, neuropeptides, and cytokines to initiate and maintain pain has been extensively studied, recent work has identified a key role for reactive oxygen and nitrogen species (ROS/RNS; nitroxidative species), including superoxide, peroxynitrite, and hydrogen peroxide. In this review we describe how nitroxidative species are generated after tissue injury and the mechanisms by which they enhance neuroexcitability in pain pathways. Finally, we discuss potential therapeutic strategies for normalizing nitroxidative signaling, which may also enhance opioid analgesia, to help to alleviate the enormous burden of pathological pain.
组织损伤可引发神经元、神经胶质细胞和免疫细胞之间的双向信号传导,从而产生并放大疼痛。虽然神经递质、神经肽和细胞因子引发和维持疼痛的能力已得到广泛研究,但最近的研究发现活性氧和氮物种(ROS/RNS;氮氧化物种),包括超氧化物、过氧亚硝酸盐和过氧化氢,也发挥着关键作用。在本综述中,我们描述了组织损伤后氮氧化物种是如何产生的,以及它们增强疼痛通路中神经兴奋性的机制。最后,我们讨论了使氮氧化信号正常化的潜在治疗策略,这也可能增强阿片类药物的镇痛作用,以帮助减轻病理性疼痛的巨大负担。