Open AccessActivated Microglia in Nociception
Author(s) -
Howard S. Smith
Publication year - 2010
Publication title -
pain physician
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 99
eISSN - 2150-1149
pISSN - 1533-3159
DOI - 10.36076/ppj.2010/13/295
Subject(s) - microglia , neuropathic pain , medicine , tlr4 , neuroscience , nociception , nerve injury , chemokine , inflammation , receptor , pharmacology , anesthesia , immunology , biology
Microglial cells appear to play a vital role in the initiation of certainneuropathic pain states. In order to initiate neuropathic pain, microglianeed to be activated. Microglia activation in the spinal cord involves bothhypertrophy as well as hyperplasia, progressing through a hypertrophicmorphology, with thickened and retracted processes (observed within thefirst 24 hours after nerve injury), and an increase in cell number (observedaround 2–3 days after nerve injury). There seems to be at least 5 major pathsto activate microglia. These 5 pathways will be discussed and are identifiedby their main signaling mediator and/or receptor which include fractalkine,interferon-gamma, monocyte chemoattractant protein-1, TLR4, and P2X4.Thus, one or more of these mediators/pathways which lead to microglialactivation might contribute to neuropathic pain. A greater appreciation ofthe roles of various mediators/paths which activate microglia might help leadto future novel therapeutic targets in efforts to ameliorate severe symptomsof neuropathic pain.Key words: microglial cells, glia, C-fiber nociceptors, neuropathic pain,hypertrophy, hyperplasia