A toxin from the venom of the predator snail Conus textile modulates ionic currents in Aplysia bursting pacemaker neuron.

Conus textile crude venom and a peptide component ('King Kong' toxin) purified from this venom, alter membrane excitability of Aplysia neurons. Venom, applied to the medium bathing an abdominal ganglion, changes dramatically the electrical activity of bursting pacemaker neuron. The effects on bursting neuron R15 was examined in current-clamp and voltage-clamp modes. A dual phase effect of both the venom and the purified toxin were observed. The first phase starts immediately after venom or toxin application and is observed as an increase in membrane excitability, resulting in an enhancement of bursting. The second phase begins about 15 min later and consists of a long-lasting hyperpolarization. The dual phase effect of the venom and the toxin persists even when synaptic input is eliminated either by axotomy, or by recording from freshly dissociated neurons or from neurons in primary cell culture. The ionic currents affected are an inward current, INSR, which is activated upon depolarization and an anomalously rectifying potassium current, IR, which is activated upon hyperpolarization. In the first phase of toxin action INSR is increased. In the second phase both the venom and the toxin block INSR and increase IR. The toxin effects may be due to complex alteration of one or more second messenger cascades rather than a direct action on ion channels.