Contribution of glial cells to neuropathic pain

In recent years increasing evidence has emerged that not only neuronal elements, but also glial cells play an important role in the initiation and maintenance of neuropathic pain. In experimental pain states in animals, astrocytes and microglia are activated by neuronal transmitters including substance P and glutamate (Wieseler-Frank et al. 2005). In turn, glial cells release proinflammatory cytokines and other sensitizing compounds that promote long-lasting spinal hyperexcitability and therefore are key factors for the transition from acute to chronic pain (Chacur et al. 2009). For example, brain-derived neurotrophic factor (BDNF) released from activated glial cells fosters the reduction of the potassium chloride exporter (KCC2) in lamina I neurons. A consequence is an alteration of chloride homeostasis in these cells leading to depolarization. This shift inverts the polarity of currents activated by GABA which become excitatory and thus enhance the sensitization of projecting neurons (Coull et al. 2003, 2005).

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