Research by Yves De Koninck and Robert Bonin at Laval University in Quebec exploits the similarities between memory formation and chronic pain in the nervous system and comes up with a possible way to “erase” chronic pain.
Let’s say that you accidentally prick your finger. Current thinking about the way that your body perceives the pain goes something like this: When the nerve cell in your finger senses the painful stimulus (the prick), it transmits an electrical signal along its length toward your spinal cord which will carry that message to your brain. But the nerve cells in the spinal cord aren’t continuous; there are small gaps (synapses) between them that the electrical signal can’t travel across. To transmit their messages onward, nerve cells employ a chemical messenger that carries the signal across the gap, from one cell to the next.
Usually, the pain from a pricked finger doesn’t last long, but that’s not the case for some chronic pain patients. Because chronic pain is pain that doesn’t turn off when it should, chronic pain patients can suffer from extra and longer-lasting sensitivity (hyperalgesia) to what in other people would be just a pricked finger.
Research published by Yves De Koninck and Robert Bonin of Laval University offers a hope for breaking the cycle of chronic neuropathic pain. It does this by exploiting the similarity between the ways that memory and pain work.
Although memory formation occurs in the brain, not spinal cord, the mechanisms at play have much in common with pain perception. It’s widely accepted that the transmission of nerve signals across synapses in the brain strengthens the connection between nerve cells and results in memory formation. Research done on mice has shown that disrupting the chemical mechanism that allows nerve cells to communicate during memory formation prevents memories from forming. More recently, researchers at NYU discovered that the same technique not only prevents new memories, it can actually be used to erase old memories. Usually when a memory is recalled, it is strengthened. But the NYU researchers found that if the drug anisomycin, which blocks the synthesis of certain proteins, is given when a memory is recalled, the memory is erased instead.
In their paper “A spinal analog of memory reconsolidation enables reversal of hyperalgesia” (Nature Neuroscience, July 2014), De Koninck and Bonin reveal that this trick can also work to erase pain, at least in mice. Mice were given an injection of the drug capsaicin in their paws and experienced increased sensitivity to pain for hours. (Capsaicin, which is derived from chili peppers, causes the sensation of pain without cell damage.) But when the mice were given a second injection of capsaicin, this time accompanied by anisomycin, their increased susceptibility to pain decreased by 70%. So by accompanying a repeat painful experience with the addition of anisomycin, De Koninck and Bonin actually caused the mice to feel less pain instead of more.
Of course it’s very early to begin to talk about how these results could translate to treatment for humans, but they do open new avenues for drug research and a distant hope for the treatment hyperalgesia.
This blog post owes much to the excellent article “Teaching the Nervous System to Forget Chronic Pain” by Eleanor Nelsen (see http://www.pbs.org/wgbh/nova/next/body/chronic-pain/)