p38 MAPK, microglial signaling, and neuropathic pain

doi:10.1186/1744-8069-3-33

Molecular Pain

Volume 3

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p38 MAPK, microglial signaling, and neuropathic pain

Ru-Rong Ji and Marc R Suter

Pain Research Center, Department of Anesthesiology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

author email corresponding author email

Molecular Pain 2007, 3:33doi:10.1186/1744-8069-3-33


Published:	1 November 2007

Abstract

Accumulating evidence over last several years indicates an important role of microglial cells in the pathogenesis of neuropathic pain. Signal transduction in microglia under chronic pain states has begun to be revealed. We will review the evidence that p38 MAPK is activated in spinal microglia after nerve injury and contributes importantly to neuropathic pain development and maintenance. We will discuss the upstream mechanisms causing p38 activation in spinal microglia after nerve injury. We will also discuss the downstream mechanisms by which p38 produces inflammatory mediators. Taken together, current data suggest that p38 plays a critical role in microglial signaling under neuropathic pain conditions and represents a valuable therapeutic target for neuropathic pain management.