antillatoxin activates voltage-gated sodium channels, thus increasing sodium influx into the cell. it is hypothesized that atx creates the increase in sodium influx by altering the voltage-gating properties of the channel. the toxin might change the voltage dependence of inactivation or augment the rate of recovery from inactivation. the effect is concentration dependent, with similar potency for the rnav1.2, rnav1.4 and rnav1.5 α-subunit types of sodium channels.