Abstract
Scorpion toxins significantly disrupt the normal function of ion channels, leading to abnormal nerve excitability and severe pain responses. Notably, α-type sodium channel toxins (α-NaTx) and β-type sodium channel toxins (β-NaTx) target sodium channels through distinct mechanisms: α-NaTx prolongs channel opening, while β-NaTx lowers the activation threshold, resulting in persistent nerve overexcitation and heightened pain. This review synthesizes current knowledge on pain-inducing venom peptides isolated from various scorpion species, elucidating the underlying molecular mechanisms involving ion channels. Furthermore, it explores the potential applications of these toxins in scientific research and drug development, highlighting their significance in advancing our understanding of pain mechanisms and facilitating the development of novel analgesic therapies.