News
Douglas researchers identify new pain protein
2006-10-25
Even the slightest touch may cause tears for those who suffer from hyperalgesia – an extreme sensitivity to pain. Thanks to new research findings from the Douglas Hospital Research Centre (DHRC), treatment for this condition may be one step closer. The study, published in a recent issue of the prestigious scientific magazine Proceedings of the National Academy of Sciences, identifies adrenomedullin (AM) as a powerful pain-inducing protein.
“Previous research characterized AM as protein with many biological functions, including cell proliferation and inflammation,” says principal investigator Rémi Quirion, PhD, Scientific Director of the DHRC and of the Institute of Neurosciences, Mental Health and Addiction (CIHR) and Professor of Psychiatry at McGill University. “Our findings are the first to demonstrate its significant role in pain modulation, particularly in long-lasting heat hypersensitivity and hyperalgesia.”
Quirion and his colleagues used an animal model to characterize the pain-inducing role of AM. Using biochemical and microscopy techniques, they demonstrated that the AM protein is present is the nerve endings of cells capable of perceiving pain. By injecting AM into rats, a gentle stimulus that is not normally considered painful became able of eliciting a painful response. Conversely, blocking or intercepting the AM signaling reversed this hyperalgesic effect.
“Our results clearly demonstrate this new pain-inducing role for AM,” says Quirion. “This is ground-breaking and opens a new avenue for pain research and treatment.”
Online Article
“Previous research characterized AM as protein with many biological functions, including cell proliferation and inflammation,” says principal investigator Rémi Quirion, PhD, Scientific Director of the DHRC and of the Institute of Neurosciences, Mental Health and Addiction (CIHR) and Professor of Psychiatry at McGill University. “Our findings are the first to demonstrate its significant role in pain modulation, particularly in long-lasting heat hypersensitivity and hyperalgesia.”
Quirion and his colleagues used an animal model to characterize the pain-inducing role of AM. Using biochemical and microscopy techniques, they demonstrated that the AM protein is present is the nerve endings of cells capable of perceiving pain. By injecting AM into rats, a gentle stimulus that is not normally considered painful became able of eliciting a painful response. Conversely, blocking or intercepting the AM signaling reversed this hyperalgesic effect.
“Our results clearly demonstrate this new pain-inducing role for AM,” says Quirion. “This is ground-breaking and opens a new avenue for pain research and treatment.”
Online Article