Bukatoxin

The region between 52 and 56 in the amino acid sequence of bukatoxin, the ⁵²PDKVP ⁵⁶ loop, interacts with the neurotoxin receptor site 3, which is located on the extracellular loop of sodium channels that connects the S3 and S4 segments on the domain IV.^[3] Specifically, the tripeptide segment ⁵³ DKV ⁵⁵, which forms a surface loop that is available for binding, is suggested to play a significant role in the blocking of the inactivation of sodium channels. Other residues that could contribute to the binding of bukatoxin to the neurotoxin receptor site 3 of the sodium channels are the Val ¹ and Asp ⁹, which reside in the same surface loop.^[1] The binding of bukatoxin is thought to lead to blocking of conformational changes in the sodium channel, by preventing the outward movement of the IVS4 transmembrane segment during depolarization. As a result, inactivation of the channel becomes slower, leading to a broadened action potential.^[3]

It has been shown that relaxation of carbachol-precontracted rat anococcygeous muscle occurs through the binding of bukatoxin to sodium channels, suggesting that bukatoxin has a muscle relaxation effect. Bukatoxin produces the effects by mediating the activation of nitrergic nerve fibers,^[1] most likely via an effect on presynaptic sodium channels.^[1][4][5] Muscle relaxation effects also arise in rabbit corpus cavernosum, but the mechanisms are not sodium channel-mediated and not completely elucidated yet.^[6]