Coderre T J
Département de Médecine, Université de Montréal, Quebec, Canada.
Mol Neurobiol. 1993 Fall-Winter;7(3-4):229-46. doi: 10.1007/BF02769177.
Increased pain sensitivity (hyperalgesia) and persistent nociception following peripheral tissue injury depends both on an increase in the sensitivity of primary afferent nociceptors at the site of injury (peripheral sensitization), and on an increase in the excitability of neurons in the central nervous system (central sensitization). We will review evidence that central sensitization, and the persistent nociception it leads to, are dependent on an action of glutamate and aspartate at excitatory amino acid (EAA) receptors. Additional evidence will be presented implicating a role of various intracellular second messengers that are coupled to EAA receptors (nitric oxide, arachidonic acid, and protein kinase C) to central sensitization and persistent nociception following tissue injury. Finally, we will examine the evidence for a contribution of molecular events, including noxious stimulus-induced expression of immediate-early genes such as c-fos to persistent nociception.
外周组织损伤后疼痛敏感性增加（痛觉过敏）和持续性伤害感受，既取决于损伤部位初级传入伤害感受器敏感性的增加（外周敏化），也取决于中枢神经系统中神经元兴奋性的增加（中枢敏化）。我们将综述相关证据，即中枢敏化及其导致的持续性伤害感受，依赖于谷氨酸和天冬氨酸在兴奋性氨基酸（EAA）受体上的作用。还将呈现其他证据，表明与EAA受体偶联的各种细胞内第二信使（一氧化氮、花生四烯酸和蛋白激酶C）在组织损伤后的中枢敏化和持续性伤害感受中发挥作用。最后，我们将研究分子事件的相关证据，包括有害刺激诱导的即刻早期基因（如c-fos）表达对持续性伤害感受的影响。
