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Tarantula venom and chili peppers target same pain sensor

der activated TRPV1, but they did not pinpoint which peptides were responsible.

The fact that a second spider venom triggered a capsaicin receptor suggests that a variety of spider species may have evolved the ability to use such toxins to target heat- and pain-sensing neuron receptors, the scientists conclude.

"It is fascinating that plants and animals have evolved the same anti-predatory mechanism to generate noxious sensations," Julius said. "These toxins are incredibly useful for understanding how ion channels of the nervous system work. They give us clues as to how specific activators or blockers on these channels can be designed to treat persistent pain ?from arthritis, bladder infections, or other diseases."

The researchers determined the venom peptides' effect in neuron cell cultures, measuring the tell-tale rush of calcium ions when the venom peptides contacted the TRPV1 capsaicin receptor. They also showed that synthetic versions of the venom peptides activated the receptor. In studies with mice, they found that normal animals flinched when their paws were exposed to the peptides, which they call vanillotoxins. Mice genetically engineered to lack capsaicin receptors did not respond.


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Source:University of California - San Francisco


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