Pain is an adaptive trait that warns of tissue damage for the survival purpose. Reduce of pain sensitivity may put animals in danger of injury and death from environmental threats. However, there is an exception--- desert-dwelling grasshopper mice have evolved resistance to the pain-inducing venom from its prey, bark scorpions. What is the molecular mechanism underlying this pain resistance? It turns out that the pain-transmitting sodium channel of grasshopper mice, Nav1.8, has few amino acid different from other mammals. Therefore, rather than blocking the binding of bark scorpion toxins, the amino acid variants promotes the venom binding and inhibit Na+ current to block the transmission of the pain signals. This finding shed the new light on analgesic therapy.
A review about different types of sodium channel in pain
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