Delta-conotoxins bind to site 6 of voltage-gated sodium channels (Nav) and inhibit the inactivation process. This toxin shows weak effects on rNav1.2/SCN2A (EC(50)=2.9 uM), rNav1.4/SCN4A (EC(50)=5.2 uM), hNav1.7/SCN9A (EC(50)=1.9 uM) and rNav1.7/SCN9A (EC(50)=6.4 uM) (PubMed:10627583). In vivo, this toxin shows different effects. In mice, injection of this toxin causes hyperactivity, rapid running, limb extension, and death. In fish, the peptide elicites spurts of rapid swimming, with twisted motions, quivering fins and the lockjaw extended mouth syndrome. Rigid paralysis and death are observed at higher doses. In mollusks, this peptide is inactive. Injection of this peptide together with the kappa-conotoxin PVIIA causes the sudden tetanus of prey (STOP) syndrome, which is a single, lethal 'fin-pop' in envenomed fish. Expressed by the venom duct. The presence of a 'disulfide through disulfide knot' structurally defines this protein as a knottin. The cysteine framework is VI/VII (C-C-CC-C-C). The difference between delta-conotoxin PVIA and [deamido]-delta-conotoxin PVIA lies in the state of amidation of Gly-80. Belongs to the conotoxin O1 superfamily.