Hansson E
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
Acta Physiol (Oxf). 2006 May-Jun;187(1-2):321-7. doi: 10.1111/j.1748-1716.2006.01568.x.
An injury often starts with acute physiological pain, which becomes inflammatory or neuropathic, and may sometimes become chronic. It has been proposed recently that activated glial cells, astrocytes and microglia within the central nervous system could maintain the pain sensation even after the original injury or inflammation has healed, and convert it into chronic by altering neuronal excitability. Glial cell activation has also been proposed to be involved in the phenomenon of spread of pain sensation ipsilaterally or to the contralateral side (i.e. mirror image pain). Substance P and calcitonin gene-related peptide, released due to an inflammatory process, interact with the endothelial cells of the blood-spinal cord and blood-brain barriers. The barriers open partially and substances may influence adjacent glial cells. Such substances are also released from neurones carrying the 'pain message' all the way from the injury to the cerebral cortex. Pro-inflammatory cytokines may be released from the microglial cells, and astroglial Ca2+-transients or oscillations may spread within the astroglial networks. One theory is that Ca2+-oscillations could facilitate the formation of new synapses. These new synapses could establish neuronal contacts for maintaining and spreading the pain sensation. If this theory holds true, it is possible that Ca2+ waves, production of cytokines and growth factors could be modified by selective anti-inflammatory drugs to achieve a balance in the activities of the different intercellular and intracellular processes. This paper reviews current knowledge about glial mechanisms underlying the phenomena of chronic pain and spread of the pain sensation.
损伤通常始于急性生理性疼痛，随后转变为炎症性或神经性疼痛，有时还会发展为慢性疼痛。最近有人提出，中枢神经系统内被激活的神经胶质细胞，即星形胶质细胞和小胶质细胞，即使在最初的损伤或炎症愈合后仍可维持疼痛感觉，并通过改变神经元兴奋性将其转变为慢性疼痛。神经胶质细胞激活还被认为与疼痛感觉同侧或对侧扩散（即镜像疼痛）现象有关。由炎症过程释放的P物质和降钙素基因相关肽，与血脊髓屏障和血脑屏障的内皮细胞相互作用。这些屏障会部分打开，物质可能会影响相邻的神经胶质细胞。此类物质也会从将“疼痛信号”从损伤部位一路传递至大脑皮层的神经元中释放出来。促炎细胞因子可能从小胶质细胞中释放出来，星形胶质细胞的Ca2+瞬变或振荡可能会在星形胶质细胞网络内传播。有一种理论认为，Ca2+振荡可能会促进新突触的形成。这些新突触可以建立神经元联系，以维持和传播疼痛感觉。如果这一理论成立，那么Ca2+波、细胞因子和生长因子的产生可能会被选择性抗炎药物改变，从而在不同细胞间和细胞内过程的活动中实现平衡。本文综述了目前关于慢性疼痛和疼痛感觉扩散现象背后神经胶质机制的知识。
