Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/43166
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Glia as the "bad guys": Implications for improving clinical pain control and the clinical utility of opioids
Author: Watkins, L.
Hutchinson, M.
Ledeboer, A.
Wieseler-Frank, J.
Milligan, E.
Maier, S.
Citation: Brain Behavior and Immunity, 2007; 21(2):131-146
Publisher: Academic Press Inc
Issue Date: 2007
ISSN: 0889-1591
1090-2139
Abstract: Within the past decade, there has been increasing recognition that glia are far more than simply “housekeepers” for neurons. This review explores two recently recognized roles of glia (microglia and astrocytes) in: (a) creating and maintaining enhanced pain states such as neuropathic pain, and (b) compromising the efficacy of morphine and other opioids for pain control. While glia have little-to-no role in pain under basal conditions, pain is amplified when glia become activated, inducing the release of proinflammatory products, especially proinflammatory cytokines. How glia are triggered to become activated is a key issue, and appears to involve a number of neuron-to-glia signals including neuronal chemokines, neurotransmitters, and substances released by damaged, dying and dead neurons. In addition, glia become increasingly activated in response to repeated administration of opioids. Products of activated glia increase neuronal excitability via numerous mechanisms, including direct receptor-mediated actions, upregulation of excitatory amino acid receptor function, downregulation of GABA receptor function, and so on. These downstream effects of glial activation amplify pain, suppress acute opioid analgesia, contribute to the apparent loss of opioid analgesia upon repeated opioid administration (tolerance), and contribute to the development of opioid dependence. The potential implications of such glial regulation of pain and opioid actions are vast, suggestive that targeting glia and their proinflammatory products may provide a novel and effective therapy for controlling clinical pain syndromes and increasing the clinical utility of analgesic drugs.
Keywords: Interleukin-1; Microglia; Astrocytes; Neuropathic pain; Morphine; Methadone; Analgesia; Tolerance; Dependence; Withdrawal
RMID: 0020076178
DOI: 10.1016/j.bbi.2006.10.011
Description (link): http://www.elsevier.com/wps/find/journaldescription.cws_home/622800/description#description
Appears in Collections:Earth and Environmental Sciences publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.