News in Brief: Centipede venom fights pain
A chemical found in centipede venom wipes out pain just as well as morphine does, a study in mice shows.
Ssm6a is a protein fragment that blocks a pain-sensing channel called Nav1.7. Pharmaceutical companies are in hot pursuit of molecules that do the same thing (SN: 6/30/12, p. 22). Because the channel resides mainly in the body’s peripheral nerves, compounds that block Nav1.7 shouldn’t cause dizziness, drowsiness or other side effects of current pain-relief drugs that affect neurons in the brain.
This discovery seems related to the sodium channels mentioned in another research article:
Mutation in Nav1.9 Sodium Channel Linked to Pain Insensitivity in People | Pain Research Forum
The new findings are particularly surprising because they indicate that increased activity in Nav1.9 leads to pain insensitivity found in people with congenital insensitivity to pain.
Unexpectedly, gain of function in channel appears to lead to loss of pain sensation
Sodium channels expressed in nociceptors, most notably Nav1.7, have recently emerged as important players in pain signaling and as the culprit in several pain disorders
mutations that make Nav1.7, or its cousin Nav1.8 more active have the opposite effect, leading to pain conditions including inherited erythromelalgia and small fiber neuropathy
The consequences of the mutation arise not only from how it alters the function of the channel protein—in this case, voltage dependence of gating—but also how it interacts with the specialized combination of other ion channels and signaling molecules that populate each cell type, including human pain-sensing neurons of the DRG.
Studying pain from “the other side” in people who cannot feel any pain at all could be a fruitful approach to research and yield clues about how pain is transmitted. The better we understand the pain process, the more likely we are to find a weak link or specific mechanism we can attack to break the vicious cycle of chronic pain.