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.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Chemokines / metabolism
-
Chronic Disease
-
Disease Models, Animal
-
Humans
-
Inflammation Mediators / metabolism*
-
Mice
-
Microglia / drug effects
-
Microglia / metabolism*
-
Neuralgia / classification
-
Neuralgia / drug therapy
-
Neuralgia / metabolism*
-
Pain Measurement / methods
-
Pyrazoles / metabolism
-
Pyridines / metabolism
-
Rats
-
Receptors, Chemokine / metabolism
-
Signal Transduction*
-
Spinal Cord / cytology
-
Spinal Cord / metabolism
-
Spinal Nerves / injuries
-
Spinal Nerves / metabolism
-
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
-
p38 Mitogen-Activated Protein Kinases / metabolism*
Substances
-
Chemokines
-
FR 167653
-
Inflammation Mediators
-
Pyrazoles
-
Pyridines
-
Receptors, Chemokine
-
p38 Mitogen-Activated Protein Kinases