Tarantulas are, for most people, the stuff of nightmares – but their venom is helping scientists find a drug to relieve irritable bowel syndrome.
Researchers from Australia and the US isolated a toxin from the venom of West African tarantula Heteroscodra maculata and found it kept pain nerves in the colon “switched on” and transmitting to pain signal the brain. This finding could point the way to a new drug.
Study co-author Stuart Brierley from the University of Adelaide explains that irritable bowel syndrome, or IBS, is akin to food poisoning, but experienced on a daily or weekly basis. Symptoms include diarrhoea, lethargy and chronic gut pain.
“It’s a really debilitating disease. In terms of quality of life, it’s pretty bad,” he says. “There is a lack of treatments for IBS at the moment, so anything we can do to help these poor patients is really significant.”
Abdominal pain, a key symptom of IBS, is an example of mechanical pain. When the bowel moves, it stimulates sensitive nerve endings.
If you zoom in on the nerve cells, they have channels, like tiny gates, to let chemicals such as sodium in and out of the cell. When sodium rushes into the cell, it initiates and perpetuates an electrical impulse. In a pain nerve cell, that signals pain to the brain.
Brierley and colleagues found that a toxin from tarantula venom specifically activates one of these mechanical pain channels, dubbed Nav1.1.
They removed tissue from healthy mice and mice with IBS, complete with nerve fibres attached so they could track pain signals.
When they dropped a little of the tarantula toxin on the nerve endings in the bowel, they saw the pain signal shooting through the IBS mouse nerves was much stronger than the healthy mouse tissue.
The toxin targeted the Nav1.1 channel, showing scientists clearly how it operates for the first time. Once the channel was open, the toxin prevented the channel closing again, forcing the nerve’s pain signal to stay switched on.
Knowing this could, one day, provide IBS patients with targeted pain relief.
“Now that we know that Nav1.1 is one of the underlying causes of chronic abdominal pain, we can start to look at mechanisms to essentially shut that channel down so that chronic pain won’t be signalled,” Brierley says.
The study was published in Nature.