The ERK/MAPK pathway, as a target for the treatment of neuropathic pain.
Peripheral nerve injury produces neuropathic pain as well as phosphorylation of mitogen activated protein kinase (MAPK) family in dorsal root ganglia (DRG) and dorsal horn. Following nerve injury, phosphorylation of extracellular signal-regulated protein kinase (ERK), an important member of this family, is sequentially increased in neurons, microglia and astrocytes of the dorsal horn and gracile nucleus, and in injured large DRG neurons. Nerve injury-induced phosphorylation of ERK occurs early and is long-lasting. In several animal models of neuropathic pain, MEK inhibitors, known to suppress the synthesis of ERK, have proven effective to alleviate pain at various time points. Thus, the regulation of ERK/MAPK can be considered as a promising therapeutic target for the treatment of neuropathic pain.
Ma
Weiya
W
Douglas Hospital Research Center, McGill University, Verdun, Montreal, Quebec, H4H 1R3, Canada.
Quirion
Remi
R
D000700:Analgesics / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D010146:Pain / Q000188:drug therapy* / Q000201:enzymology / Q000378:metabolism; D010523:Peripheral Nervous System Diseases / Q000188:drug therapy* / Q000201:enzymology / Q000378:metabolism; D020886:Somatosensory Disorders / Q000188:drug therapy* / Q000201:enzymology / Q000378:metabolism
D000700:Analgesics; D048049:Extracellular Signal-Regulated MAP Kinases