Abstract
Classically, pain is viewed as being mediated solely by neurons. However, recent research has shown that activated glial cells (astrocytes and microglia) within the spinal cord amplify pain. These nonneuronal cells play a major role in the creation and maintenance of pathological pain. Glia become activated by immune challenges (viral or bacterial infection) and by substances released by neurons within the pain pathway. Activated glia amplify pain by releasing proinflammatory cytokines. Taken together, research findings suggest a novel approach to human pain control that targets glia. In addition, it is likely that such glial-neuronal interactions are not unique to pain, but rather reflect a general rule of sensory processing.
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