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Targeting glial activation for treating chronic pain and improving opioid efficacy (84.3)
Author(s) -
Watkins Linda
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.84.3
Subject(s) - neuropathic pain , opioid , medicine , neuroscience , chronic pain , central nervous system , morphine , pharmacology , anesthesia , psychology , receptor , physical therapy
Research spanning 20 years into the mechanisms of neuropathic pain has defined a new therapeutic target: glial cell activation. Glial cells surround nerve cells throughout the central nervous system, interacting with the nerve cells and responding to their signaling. In neuropathic pain, glial cells become activated, causing them to release substances that pathologically amplify pain. This new understanding has also provided an explanation for the clinical experience that opioids often have pain‐promoting side effects. Opioid administration causes glial activation, which paradoxically opposes the pain‐modulating effect of opioids. Reversal of the pro‐inflammatory activation of glia would thus not only reverse neuropathic pain in general but should also enhance the clinical efficacy of morphine and other opioids.