Propagating calcium spikes in an axon of Aplysia.

1. Intracellular recordings were obtained from the axon of the giant neurone R2 of Aplysia in order to study the ionic dependency of action potentials. 2. The overshoot potential of the axon spike increases with Na concentration in the manner predicted for a Na electrode. The maximum rate of rise (Vm) is linearly related to Na concentration. The overshoot potential is insensitive to Ca concentration at Na concentrations as low as 250 mM. 3. Tetrodotoxin (TTX) or replacement of Na with Tris abolishes action potentials in the axon but not soma of R2. Addition of 4-aminopyridine to a Na-free solution permits axon spikes to be generated. These action potentials are blocked by 30 mM-Co2+, but not by TTX. The overshoot potential and Vm of these action potentials increase monotonically with Ca concentration. 4. Axonal action potentials can be generated when an equimolar concentration of Sr is substituted for all of the Ca and Mg in Na-free medium. These action potentials are abolished by 30 mM-Ca2+ or mM-Co2+, and increase with Sr concentration. 5. TTX-resistant Ba spikes can similarly be elicited in R2 axon. These action potentials are reduced by Ca, Co, or Cd, and enhanced by raising the Ba concentration. 6. The Vm of Na spikes in the absence of Ca is greater in the axon than in the soma of R2, whereas the Vm of divalent spikes is greater in the soma. 7. During repetitive stimulation the axon spikes incrase in duration. This broadening is inhibited by replacing Ca in the bath with Mn or by the addition of 30 mM-CoCl2, and is enhanced by raising the Ca concentration by 30 mM. 8. The action potention of R2 axon has a mixed Na/Ca dependency. The density of Ca current may be greater in the some than in the axon of this cell.