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Spinal p38 mitogen‐activated protein kinase mediates allodynia induced by first‐degree burn in the rat
Author(s) -
Sorkin Linda,
Svensson Camilla I.,
JonesCordero Toni L.,
Hefferan Michael P.,
Campana W. Marie
Publication year - 2009
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21905
Subject(s) - allodynia , p38 mitogen activated protein kinases , mapk/erk pathway , ampa receptor , microglia , protein kinase a , neuroscience , kainate receptor , noxious stimulus , spinal cord , kinase , medicine , receptor , hyperalgesia , pharmacology , nociception , chemistry , anesthesia , biology , microbiology and biotechnology , glutamate receptor , inflammation
Activation of p38 mitogen‐activated protein kinase (MAPK) in the spinal cord has been implicated in the development and maintenance of pain states. In this study, we tested whether p38 MAPK is involved in the response to first‐degree burn of the hind paw. This injury induces central sensitization leading to tactile allodynia and is mediated by activation of Ca 2+ permeable AMPA/kainate receptors through PKC and PKA. We demonstrate that p38 MAPK is rapidly and robustly activated in the superficial spinal dorsal horn after mild thermal injury to the hind paw. Activated p38 MAPK was localized primarily to microglia and to a lesser extent in oligodendrocytes and lamina II neurons. Astrocytes were not involved in the p38 MAPK response. Intrathecal pretreatment of pharmacological inhibitors of p38 MAPK (SB203580, SD‐282) dose‐dependently blocked development of tactile allodynia, a characteristic of the first‐degree burn model. The effects of the inhibitors on tactile allodynia were lost when they were administered after injury. These studies identify p38 MAPK as a major mediator of tactile allodynia, most likely activated downstream of AMPA/kainate receptors. © 2008 Wiley‐Liss, Inc.