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Do glial cells control pain?

Published online by Cambridge University Press:  24 April 2008

Marc R. Suter ,
Yeong-Ray Wen ,
Isabelle Decosterd  and
Ru-Rong Ji
Marc R. Suter*
Affiliation:
Pain Research Center, Department of Anesthesiology, Brigham and Women's Hospital and Harvard Medical School, Boston, USA
Yeong-Ray Wen
Affiliation:
Department of Anesthesiology, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
Isabelle Decosterd
Affiliation:
Anesthesiology Pain Research Group, Anesthesiology Department, University Hospital Center and University of Lausanne, Switzerland Department of Cell Biology and Morphology, University of Lausanne, Switzerland
Ru-Rong Ji*
Affiliation:
Pain Research Center, Department of Anesthesiology, Brigham and Women's Hospital and Harvard Medical School, Boston, USA
*
Correspondence should be addressed to Either Marc R Suter, MD or Ru-Rong Ji PhD, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, MRB 611, Boston, MA 02115, USA phone: +1 617 732 8852 fax: +1 617 730 2801 email: msuter1@partners.org, , email: rrji@zeus.bwh.harvard.edu
Correspondence should be addressed to Either Marc R Suter, MD or Ru-Rong Ji PhD, Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, MRB 611, Boston, MA 02115, USA phone: +1 617 732 8852 fax: +1 617 730 2801 email: msuter1@partners.org, , email: rrji@zeus.bwh.harvard.edu
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Abstract

Management of chronic pain is a real challenge, and current treatments that focus on blocking neurotransmission in the pain pathway have resulted in limited success. Activation of glial cells has been widely implicated in neuroinflammation in the CNS, leading to neurodegeneration in conditions such as Alzheimer's disease and multiple sclerosis. The inflammatory mediators released by activated glial cells, such as tumor necrosis factor-α and interleukin-1β not only cause neurodegeneration in these disease conditions, but also cause abnormal pain by acting on spinal cord dorsal horn neurons in injury conditions. Pain can also be potentiated by growth factors such as brain-derived growth factor and basic fibroblast growth factor, which are produced by glia to protect neurons. Thus, glial cells can powerfully control pain when they are activated to produce various pain mediators. We review accumulating evidence that supports an important role for microglial cells in the spinal cord for pain control under injury conditions (e.g. nerve injury). We also discuss possible signaling mechanisms, in particular mitogen-activated protein kinase pathways that are crucial for glial-mediated control of pain. Investigating signaling mechanisms in microglia might lead to more effective management of devastating chronic pain.

Keywords

MicrogliaMAP kinasechemokinescytokinesintracellular signalingchronic painnerve injury
Type
Review Article
Information
Neuron Glia Biology , Volume 3 , Issue 3 , August 2007 , pp. 255 - 268
Copyright
Copyright © Cambridge University Press 2008

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