Researchers at the University of California, Davis have discovered a "cross-talk" between two major biological pathways that involve painresearch that may pave the way to new approaches to understanding and controlling chronic pain.
And they did it with something old, new, practical and basic.
The newly published research reveals that analgesia mediated by inhibitors of the enzyme, soluble epoxide hydrolase (sEH), is dependent on a pain-mediating second messenger known as cyclic adenosinemonophosphate or cAMP.
"The interaction of many complex biological pathways is essential for the development of persistent pain, whether inflammatory or neuropathic," said lead researcher Bora Inceoglou of the Bruce Hammock lab, UC Davis Department of Entomology. Inflammatory pain includes arthritis, and neuropathic pain is linked to diabetes and other diseases, and trauma.
"Pain is a major health concern and painkiller medications or analgesics do different things," Inceoglu said. Painkilling medications may target the pain, but have side effects or lack a broad-spectrum efficacy.
The collaborative study, the work of scientists in the UC Davis Department of Entomology, UC Davis Cancer Center, UC Davis School of Medicine and the School of Veterinary Medicine, is published in the March 7th early edition of the Proceedings of the National Academy of Sciences (PNAS).
An estimated 9 percent or 30 million adults in the United States suffer from moderate to severe non-cancer related chronic pain, according to the American Pain Society.
The messenger, cAMP, relays responses and mediates the action of many biological processes, including inflammation, and cardiac and smooth muscle contraction.
The research, done on rodents and funded by the National Institutes of Health, confirmed earlier studies at UC Davis that showed stabilization of natural epoxy-fatty acids (EFAs) through inhibition of sEH reduces pain. "However, in the absence of an u
|Contact: Kathy Keatley Garvey|
University of California - Davis Health System