Could chronic pain and spread of pain sensation be induced and maintained by glial activation?
Could chronic pain and spread of pain sensation be induced and maintained by glial activation?
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DOI：
10.1111/j.1748-1716.2006.01568.x
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发表时间：
2006-05-01
影响因子：
6.3
通讯作者：
Hansson, E.
中科院分区：
文献类型：
--
作者：
Hansson, E.
损伤通常始于急性生理性疼痛，其变为炎症性或神经性疼痛，并且有时可能变为慢性疼痛。最近有人提出，中枢神经系统内激活的胶质细胞、星形胶质细胞和小胶质细胞可以在原始损伤或炎症愈合后维持疼痛感觉，并通过改变神经元的兴奋性将其转化为慢性疼痛感觉。神经胶质细胞活化也被认为与痛觉同侧或对侧扩散（即镜像疼痛）的现象有关。由于炎症过程释放的P物质和降钙素基因相关肽与血脊髓和血脑屏障的内皮细胞相互作用。屏障部分打开，物质可能影响邻近的神经胶质细胞。这些物质也会从神经元中释放出来，这些神经元将“疼痛信息”从受伤处一直传递到大脑皮层。促炎细胞因子可从小胶质细胞释放，并且星形胶质细胞Ca2+瞬变或振荡可在星形胶质细胞网络内扩散。有一种理论认为，钙振荡可以促进新突触的形成。这些新的突触可以建立神经元的联系，以维持和传播痛觉。如果这一理论成立，它是可能的，Ca2+波，细胞因子和生长因子的生产可以通过选择性抗炎药物进行修改，以实现不同的细胞间和细胞内过程的活动的平衡。本文综述了目前有关神经胶质机制的基础上的现象，慢性疼痛和蔓延的痛觉。
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.