Glia and pain: is chronic pain a gliopathy?
It is well known that there are many neuronal mechanisms that underlie chronic pain, including peripheral and central sensitisation. Aside from these processes, there is a growing understanding of the importance of non-neuronal cells, such as glial cells, as major players in chronic pain.
The aim of this paper was to provide a comprehensive review of glia and pain. Studies have shown that glial cells play an active role in diseases such as seizure, stroke, ischemia, neuropathic and inflammatory pain. The central nervous system consists of three major groups of glial cells: astrocytes, microglia, and oligodendrocytes.
Glial cells exhibit variable alterations in functions and morphologies after painful stimuli and these changes are associated with different glial states. 1) Up-regulation of glial markers and morphological changes of glia: 2) up-regulation of glial receptors: 3) Activation of intracellular signalling pathways; 4) Up-regulation of glial mediators such as cytokines, chemokines and growth factors. These glial mediators interact with neurons and can elicit pain via processes such as central and peripheral sensitization.
Most research on glial cells has been based on animal models and little is known about the role of human glia in pain. Further research is needed to provide more insight into human glia interactions and their role in chronic pain states. > From: Ru-Rong et al., Pain 154 (2013) 10-28. All rights reserved to International Association for the Study of Pain.
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