p38 MAPK, microglial signaling, and neuropathic pain

By R. Ji, M. Suter. Molecular Pain, 2007

609 citations recorded by the source corpus.

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.

Subfields: Neurology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/075f9dddebb20dd63cb2c76d17e1bafec77d0d8d

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Citations in the corpus

MAP kinase and pain (2008, background): “, 2003b), IL-1β (Ji and Suter, 2007), and iNOS (Sung et al.”
Models and mechanisms of hyperalgesia and allodynia. (2009, background): “Stimulation of dorsal roots at C-fiber intensity with low frequencies (0.05–10 Hz) (143) or higher frequencies [50 Hz (212) or 100 Hz (283, 595)] induces phosphorylation of extracellular receptor-activated kinase in superficial but not in deep spinal dorsal horn [See also Ji and Suter (214) for a re”
Glia and pain: Is chronic pain a gliopathy? (2013, background): “Although most studies have focused on glial reaction in the spinal cord and brainstem, astrocyte reaction has also been found in the forebrain, such as the anterior cingulate cortex, which contributes to affective pain [28].”
Pathological and protective roles of glia in chronic pain (2009, background): “During chronic neuropathic conditions, astrocytes remain activated in response to the initial microglia-derived inflammatory factor”
Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, positive): “Activated microglia produce and release trophic factors, neurotransmitters, cytokines, and reactive oxygen species(263,361) and appear to play an essential step in the development of pain after nerve injury by triggering central sensitization through their interaction with neurons.(133,160,162,201,2”