Wise Young
09-27-2001, 03:21 PM
Spinal cord glia: new players in pain [Topical review]
Linda R. Watkins, Erin D. Milligan and Steven F. Maier
Pain, 2001, 93:3:201-205
Manuscript received 01 June 2001 Accepted 12 June 2001;
Abstract
There is no abstract for this article. The text below is the first paragraph of text within the article.
At the level of the spinal cord, pathological pain is classically viewed as being created and maintained solely by neurons. Glia (microglia and astrocytes) were not considered to play a role as they were not thought to function in cell-to-cell signaling. However, there is mounting evidence that glia within the spinal cord dorsal horns create and maintain pathological pain. Spinal cord glia are now implicated in exaggerated pain states created by such diverse manipulations as subcutaneous inflammation, neuropathy, and spinal immune activation. Indeed, glial activation has been shown to be necessary and sufficient to create pathological pain states in laboratory animals. This review will summarize how glia become activated and how activated glia drive pathological pain states. Finally, the implications of these new findings for clinical drug development will be addressed.
Linda R. Watkins, Erin D. Milligan and Steven F. Maier
Pain, 2001, 93:3:201-205
Manuscript received 01 June 2001 Accepted 12 June 2001;
Abstract
There is no abstract for this article. The text below is the first paragraph of text within the article.
At the level of the spinal cord, pathological pain is classically viewed as being created and maintained solely by neurons. Glia (microglia and astrocytes) were not considered to play a role as they were not thought to function in cell-to-cell signaling. However, there is mounting evidence that glia within the spinal cord dorsal horns create and maintain pathological pain. Spinal cord glia are now implicated in exaggerated pain states created by such diverse manipulations as subcutaneous inflammation, neuropathy, and spinal immune activation. Indeed, glial activation has been shown to be necessary and sufficient to create pathological pain states in laboratory animals. This review will summarize how glia become activated and how activated glia drive pathological pain states. Finally, the implications of these new findings for clinical drug development will be addressed.