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In response to peripheral nerve injury, glia (microglia and astrocytes) in spinal cord become activated. This spinal glial activation has been causally linked to the induction and maintenance of neuropathic pain. The question arises as to how glia become activated as a consequence of distant injury. This chapter reviews current evidence for glial activation in response to neurotransmitters, neuromodulators, and unique neuron-to-glia signals.

Publisher Summary This chapter reviews the role of glial cells in normal physiology and pathophysiology, particularly as it relates to pain. It emphasizes on microglia and astrocytes, as these two glial populations have been the focus of the majority of studies that have investigated the role of glia in the creation and maintenance of enhanced pain states. The chapter also reviews the basic physiology and function of these glial cells under both basal and activated states. It discusses that glial activation can occur under both physiological and pathological conditions. Peripheral immune challenge is one physiological process that leads to glial activation. Peripheral inflammation and infection leads to immune activation and, consequently, to immune-to-brain communication. It also reviews that spinal cord glial cells are key contributors to the initiation and maintenance of pathological pain states. Evidence linking glia with enhanced pain, both from animal models of chronic pain conditions and from studies of morphine tolerance and the implications of their involvement for human pain management are also presented.