• L R Watkins, E D Milligan, and S F Maier.
• Dept of Psychology & the Center for Neurosciences, University of Colorado at, Boulder, CO, USA. lwatkins@psych.colorado.edu
• Trends Neurosci. 2001 Aug 1; 24 (8): 450-5.

AbstractPain is classically viewed as being mediated solely by neurons, as are other sensory phenomena. The discovery that spinal cord glia (microglia and astrocytes) amplify pain requires a change in this view. These glia express characteristics in common with immune cells in that they respond to viruses and bacteria, releasing proinflammatory cytokines, which create pathological pain. These spinal cord glia also become activated by certain sensory signals arriving from the periphery. Similar to spinal infection, these signals cause release of proinflammatory cytokines, thus creating pathological pain. Taken together, these findings suggest a new, dramatically different approach to pain control, as all clinical therapies are focused exclusively on altering neuronal, rather than glial, function.

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