A Canadian research team has identified a major gene that controls sensitivity to chronic pain. The findings are significant because they help scientists understand why people with similar disorders or injuries feel different levels of pain. They could also lead to new treatments for chronic pain.
The discoveries “point toward a new strategy for individualizing the treatment of chronic pain,” said Professor Michael Salter of The Hospital for Sick Children, which is affiliated with the University of Toronto.
Known as P2X7, the gene contains a single amino-acid change that controls the main causes of chronic pain: nerve damage and inflammation.
One function of P2X7 receptors is the formation of pores that enable molecules to pass through. When using a peptide that blocks the formation of pores, scientists learned that pain sensitivity dramatically decreased.
Researchers then looked at the genetic differences between patients suffering from osteoarthritis and chronic post-mastectomy pain. In both cases, the patients who experienced lower levels of pain had low pore formation in P2X7 receptors.
“Our findings indicate that it may be possible to develop drugs that block pores in this crucial receptor, while leaving its other function intact – thereby killing pain while minimizing side effects,” said Jeffrey Mogil, a professor of Pain Research at McGill University in Montreal.
The P2X7R gene research is published online in Nature Medicine. The US National Institutes of Health (NIH), The Krembil Foundation, the Louise and Alan Edwards Foundation, the Canadian Institutes of Health Research (CIHR) and SickKids Foundation supported the study.
A previous study out of Cambridge University in England and the University of Cadiz in Spain focused on the role of the HCN2 gene in regulating pain. In this study, researchers found that by removing the HCN2 gene they could remove neuropathic pain in mice. The study “lays the groundwork for the development of new drugs to treat chronic pain by blocking HCN2,” said Professor Peter McNaughton, lead author of the HCN2 gene study.