For many people, living with chronic pain is a way of life. Unfortunately, existing pain medications are not always effective and can be addictive, which has led to an opioid epidemic in the United States.
In their search for better therapies to manage pain, researchers are investigating the underlying mechanisms that signal and control pain in the body. A central component of this pain pathway is a protein called Nav1.7, which is present at the endings of pain-sensing nerves. Nav1.7 is known to help alert your brain when your body encounters potentially harmful stimuli, like when your hand touches a hot pan.
Past research demonstrated that people with non-functioning Nav1.7 don’t feel pain. This discovery led to the development of drugs that block Nav1.7 activity. Unfortunately, these drugs didn’t really work. It turns out that the role of Nav1.7 is more complicated than first thought.
Researchers have now found that Nav1.7 plays a second role — triggering the production and release of natural opioid compounds, like endorphins, that suppress the transmission of pain signals to the brain. People with non-functioning Nav1.7 do not feel pain and have increased expression of the genes in charge of making natural opioids.
The news story explains:
“An investigation of rat and mice nerve cells reveals the tug-of-war between Nav1.7’s pain-promoting and pain-relieving powers. Cells with nonfunctioning Nav1.7 have amped up activity in the cellular machinery that kicks off pain relief, Hucho and colleagues report. They suggest that Nav1.7 acts like the axis point in a playground seesaw. When the pain-promoting side is dialed down, the pain-relieving side becomes more dialed up than usual, and cells make more of their in-house opioids.”
This research suggests a new approach to pain management: using opiates in combination with a Nav1.7 blocker to make opiates more effective and reduce their associated side effects. However, a lot more research is needed before this work can be translated into treating people with chronic pain.
This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.