Dendrotoxin blocks potassium channels and slows sodium inactivation in Myxicola giant axons.
Dendrotoxin (DTX) is known to partially block delayed rectifier K+ channels and enhance neurotransmitter release, but no effects on Na+ channels have been reported. In voltage-clamped Myxicola axons DTX affected both the K+ and Na+ conductances. DTX blocked completely Myxicola K+ channels with a KD of 150 nM and induced slow K+ inactivation. DTX doubled the time constants for inactivation of conducting Na+ channels and gating charge immobilization without altering Na+ activation or the voltage- and time-dependent fast and slow Na+ inactivation induced by depolarizing prepulses. A selective effect on open Na+ channel inactivation provides additional evidence for kinetic models in which resting Na+ channels need not open before being inactivated.
D000818:Animals; D001369:Axons / Q000187:drug effects / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004546:Elapid Venoms / Q000494:pharmacology*; D004553:Electric Conductivity; D007473:Ion Channels / Q000187:drug effects*; D008433:Mathematics; D011077:Polychaeta; D011188:Potassium / Q000378:metabolism*
D004546:Elapid Venoms; D007473:Ion Channels; C020273:dendrotoxin; D011188:Potassium