Satellite glial cells as a target for chronic pain therapy

Sensory ganglia are essential for the transmission of sensory signals from the periphery to the central nervous system, and abnormal electrical activity in sensory neurons is a major factor in chronic pain. The main type of glial cells in these ganglia are satellite glial cells (SGCs), which surround the sensory neurons tightly. Recently it became evident that SGCs are altered profoundly after nerve injury and that they contribute to chronic pain by influencing neuronal activity. We review the biochemical, pharmacological and physiological changes that SGCs undergo in a variety of pain models, which include: augmented expression of glial fibrillary acidic protein and of proinflammatory cytokines, increased gap junctions, and reduced expression of inward rectifying K⁺ channels type K4.1. We discuss how some of these changes can lead to abnormal interactions between SGCs and neurons, and to chronic pain. We propose that these interactions may be utilized as targets for pain therapy. A most attractive option is to reduce the propagation of intercellular calcium waves in the ganglia by agents that inhibit signaling via gap junctions and purinergic P2 receptors.