They target the same pain sensorsScientists have discovered that the venom of a tarantula species from Antilles and the alkaloids (hot toxic chemicals) from the chili peppers affect the same neuronal receptors when causing the pain sensation.
It seems that plants and animals have encountered the same molecular solution to keep out predators, targeting a specific receptor on sensory cells. Understanding the way these pain- and heat-sensing neurons function could help the research on drugs that ease persistent pain in human patients, as the receptors found on mice's neurons are the same found on human neurons.
The spider's venom targets capsaicin receptor, also named TRPV1, called after capsaicin, the alkaloid from chili peppers responsible for the burning sensation.
The same team from UCSF discovered this and related receptors that provoke fire pain signals when exposed to chemicals from hot spices. The capsaicin receptor is like a channel on the neuronal surface and, when pain producing compounds reach it, the channel opens, letting into the neuron a flow of sodium and calcium ions. This produces an neuronal impulse translated by the brain as pain.
The team checked the venoms of 22 spider and scorpion species known to produce painful bites and found that the venom of the tarantula species, Psalmopoeus cambridgei (photo), triggered the response of the capsaicin receptor; three protein subunits (peptides), named vanillotoxins, were identified as responsible for activating TRPV1. The venom of a second spider species was found to activate TRPV1, but the toxic peptides from this venom are still not identified.
This second discovery supports the hypothesis that the venom of many spider species could trigger TRPV1 and similar pain receptors. "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 scientists discovered that synthetic imitators of the venom's peptides activated TRPV1. In lab experiments, mice genetically engineered to miss TRPV1 proved to be insensitive to the tarantula's venom.