If you suffer from chronic pain, there’s a good chance that your voltage-gated sodium channels are to blame. Humans have nine types of these channels, but one in particular, NaV1.7, is responsible for the sensation of some types of severe, episodic pain. I’ve explained the workings of NaV1.7 in a previous post, so go there for some background.
Scolopendra subspinipes mutilans
Photo by KENPEI, Osaka, Japan, 6/28/09.
It turns out that venom of the Chinese red-headed centipede (Scolopendra subspinipes mutilans) includes a peptide (Ssm6a) that can block NaV1.7 sodium channels. Remember, as long as the channels are closed, you can’t feel any pain. The scientists were able to reversibly block the NaV1.7 channels in mice and in human cells grown in culture. More importantly, Ssm6a offered the mice substantial pain relief, as measured by the number of times some unfortunate mice licked their aching feet. In fact, Ssm6a was significantly more effective than morphine.
The effects of Ssm6a lasted several hours, probably until the peptide was cleared by liver and kidneys. Unlike other NaV1.7 blockers, Ssm6a has little or no effect on our other eight sodium channels, making it particularly appealing as a pain drug. Previously tried drugs were less specific, and thus could not be safely administered because blocking the other sodium channels can lead to paralysis, seizure or death.
Obviously there’s a long way to go between a mouse licking its paws and a new drug on the shelf. Still, the researchers are hopeful that Ssm6a will one day help to alleviate chronic, persistent pain.