cgna slows the inactivation of tetrodotoxin-sensitive sodium currents and thereby increases the action potential duration. it preferentially binds to the closed state of the channel; it shifts the voltage-dependence of the steady-state inactivation of the sodium channels to more negative values, and also speeds up the recovery from inactivation. the toxin induces this effect acting from the extracellular side of the plasma membrane. on mammalian sodium channels, the type i toxins target receptor site 3. their effect on slowing down sodium channel inactivation leads to neurotoxic (repetitive firing) and cardiotoxic (arrhythmia) effects. the action of cgna is not use-dependent, as activation of the sodium channels by repetitive stimuli does not increase the effectiveness of cgna. the toxin has an effect on the sodium channels within 1 minute of application and is partially reversible after removal and wash out.