Activation of Erk in the anterior cingulate cortex during the induction and expression of chronic pain.
The extracellular signal-regulated kinase (Erk) activity contributes to synaptic plasticity, a key mechanism for learning, memory and chronic pain. Although the anterior cingulate cortex (ACC) has been reported as an important cortical region for neuronal mechanisms underlying the induction and expression of chronic pain, it has yet to be investigated whether or not Erk activity in the ACC may be affected by peripheral injury or in chronic pain state. In the present study, we use adult rat animal models of inflammatory and neuropathic pain and demonstrate that Erk signaling pathway in the ACC is potently activated after peripheral tissue or nerve injury. Furthermore, we demonstrate that mechanical allodynia significantly activated Erk activity at synaptic sites at two weeks after the injury. We propose a synaptic model for explaining the roles of Erk activity during different phases of chronic pain. Our findings suggest that cortical activation of Erk may contribute to both induction and expression of chronic pain.
Wei
Feng
F
Department of Biomedical Sciences, University of Maryland Dental School, Baltimore, Maryland 20201, USA. fwei@umaryland.edu
Zhuo
Min
M
D000818:Animals; D002540:Cerebral Cortex / Q000201:enzymology*; D002908:Chronic Disease; D004789:Enzyme Activation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D008297:Male; D008954:Models, Biological; D010146:Pain / Q000139:chemically induced / Q000201:enzymology*; D051381:Rats
D048049:Extracellular Signal-Regulated MAP Kinases