At the level of the spinal cord, pathological pain is clasically viewed as being developed and maintained solely by neurons. Glia (microglia and astrocyte) was not considered to play a role in pathologocal pain as they could not function in cell-to-cell synaptically signaling. Howerer, recent evidence shows the important role of spianl glia in development and maintenance of pathologocal pain. For example, spinal glia can be activated by such diverse mainpulations as subcutaneous inflammation, neuropathy, and spinal immune activation. Activated glia ralease a variety of neuroactive substances, including reactive oxygen species, nitric oxide, arachidonic acid, prostaglandins, leukotrienes, excitatory amino acid including glutamate, aspartate and cysteine, nerve growth factors, and so on. Furthermore, like immune cells, activated astrocytes and microglia release proinflammatory cytokines such as interlukin -1 and 6, tumor necrosis factor. Pre-treatment with fluorocitrate or CNI-1493, the inhibitor of glial metabolism, produces a singnifcant analgesia in pathological pain. The above evidence suggests that the activation of astrocyte of the spinal cord is necessary in development and maintenance of pathological pain...
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