TORONTO, Dec. 6 (UPI) -- A University of Toronto study indicates an inflamed injury may increase levels of a protein responsible for persistent pain.
And the enhanced levels of that protein can cause one's brain to mimic pain long after the original pain source has disappeared. The Canadian researchers said their study might have serious implications for the millions of people suffering from chronic pain.
The study demonstrates how inflammation in mice increases NR2B proteins -- proteins that facilitate nerve cell communication -- that imprint a painful response in the brain even after the stimulus is removed.
"What we're interested in uncovering are the molecular mechanisms that can turn early pain into persistent pain," said Physiology Professor Min Zhuo, the lead author of the study. "We believe that the body's inflammatory response helps to etch the initial pain into our memory."
The research is detailed in the current issue of the Journal of Neuroscience.
