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Tarantula venom points scientists to a whole new mechanical pain receptor

There exist people whose job it is to milk the venom of spiders, centipedes, and scorpions, and then do calcium imaging on cultured neurons they’ve dipped in that venom, all to find new ways in which the venom is awful. (For real; the Acknowledgements section of the report literally says, “We thank the Deutsche Arachnologische Gesellschaft and particularly I. Wendt, J. Broghammer, A. Schlosser, B. Rast, M. Luescher, C. and F. Schneider and H. Auer for providing arthropods for milking.”) The latest discovery from these brave people could lead to treatments for conditions as diverse as irritable bowel syndrome or migraines with aura. And it all stems from the way tarantula venom paralyzes its prey.

Researchers poring over the venom of the Togo Starburst tarantula discovered two new toxins that specifically target a voltage-gated ion channel called Nav1.1. The researchers named the two toxins δ-theraphotoxin- Hm1a (Hm1a) and δ-theraphotoxin-Hm1b (Hm1b). When the tarantula strikes its prey, the “main physiological target” of Hm1a and -b is Nav1.1. In concert with the heady bouquet of other components in the venom, it jams sodium channels on nerves, and thereby paralyzes the tarantula’s prey.

Earlier studies had found that mutations in Nav1.1 are linked to epilepsy, autism, and Alzheimer’s disease. There also existed a previously identified link between Nav1.1 and migraines with aura, but that’s not specifically pain either. Curiously, though, Nav1.1 is also found on nerve fibers that handle mechanical pain in mice. That’s why these researchers were interested — this is the lab that found the “wasabi receptor.” Pain is their stock in trade.

We already knew that there are many different receptors that handle many subtly different kinds of pain, including mechanical, chemical (think: ghost pepper), electrical, and thermal pain. But we didn’t know that Nav1.1 was involved in pain. The UCSF team found that blocking Nav1.1 receptors could desensitize certain nerves to that particular flavor of hurt. In a non-trivial sense, by the way, this means that the brain is receiving signals through the same pathway when someone experiences pain from IBS — or gets punched in the nose.

While the study dealt with mice, in the report the researchers immediately draw parallels to human health. In both mice and humans, the gut is thickly populated with nerve cells that express Nav1.1. Part of the study worked with mice who share many symptoms with people who have IBS. When researchers injected those mice with Hm1a, they discovered that neurons in the gut of those mice were hypersensitive to the toxin already. That meant the pain signals governed by their Nav1.1 channels were already off kilter, even in naive neurons that hadn’t been exposed to the toxin before.

Now we just need to find out whether that’s also the case in humans — and if so, how to deactivate just enough of the receptors to bring pain down to normal levels without shutting off the body’s alert system.

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