Glial cells and chronic pain.

Published

Journal Article (Review)

Over the past few years, the control of pain exerted by glial cells has emerged as a promising target against pathological pain. Indeed, changes in glial phenotypes have been reported throughout the entire nociceptive pathway, from peripheral nerves to higher integrative brain regions, and pharmacological inhibition of such glial reactions reduces the manifestation of pain in animal models. This complex interplay between glia and neurons relies on various mechanisms depending both on glial cell types considered (astrocytes, microglia, satellite cells, or Schwann cells), the anatomical location of the regulatory process (peripheral nerve, spinal cord, or brain), and the nature of the chronic pain paradigm. Intracellularly, recent advances have pointed to the activation of specific cascades, such as mitogen-associated protein kinases (MAPKs) in the underlying processes behind glial activation. In addition, given the large number of functions accomplished by glial cells, various mechanisms might sensitize nociceptive neurons including a release of pronociceptive cytokines and neurotrophins or changes in neurotransmitter-scavenging capacity. The authors review the conceptual advances made in the recent years about the implication of central and peripheral glia in animal models of chronic pain and discuss the possibility to translate it into human therapies in the future.

Full Text

Duke Authors

Cited Authors

  • Gosselin, R-D; Suter, MR; Ji, R-R; Decosterd, I

Published Date

  • October 2010

Published In

Volume / Issue

  • 16 / 5

Start / End Page

  • 519 - 531

PubMed ID

  • 20581331

Pubmed Central ID

  • 20581331

Electronic International Standard Serial Number (EISSN)

  • 1089-4098

Digital Object Identifier (DOI)

  • 10.1177/1073858409360822

Language

  • eng

Conference Location

  • United States