An inflamed injury may increase levels of a protein responsible for persistent pain, causing the brain to mimic pain long after source has disappeared, says U of T researchers. The findings could have serious implications for the millions of Canadians who suffer from chronic pain.
The study, published in the current issue of the Journal of Neuroscience, shows how inflammation in mice increases NR2B proteins – proteins that facilitate nerve cell communication – and imprint a painful response in brain even after the stimulus is removed. "What were interested in uncovering are the molecular mechanisms that can turn early pain into persistent pain," says Professor Min Zhuo of physiology, EJLB-CIHR Michael Smith Chair in Neurosciences and Mental Health and lead author of the study. "We believe that the bodys inflammatory response helps to etch the initial pain into our memory."
Normally when a mouse or a person experiences a painful event, receptors in the injury site send an electrical impulse up the spine and to the brain. The signal triggers receptors called glutamate AMPA and kainate, which flare up initially but do not directly alter the physiology of the cells. When the painful event also triggers inflammation, the nerves send extra information to the normally dormant NR2B receptors – receptors that receive messages and then produce physiological effects in the cell.
Karen Kelly | EurekAlert!
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