Post-tetanic potentiation at an identified synapse in Aplysia is correlated with a Ca2+-activated K+ current in the presynaptic neuron: evidence for Ca2+ accumulation.

We have examined the presynaptic changes underlying post-tetanic potentiation (PTP) in Aplysia by using voltage-clamp techniques combined with specific pharmacological blocking agents. The amplitude and time course of PTP parallel a slow outward clamp current that we have identified as a Ca2+-activated K+ current. Because this current is proportional to intracellular Ca2+ concentration our findings provide evidence for the "residual Ca2+ hypothesis," according to which PTP is caused by the accumulation of intracellular Ca2+ after tetanus. To obtain further evidence for this mechanism we injected EGTA intracellularly and found that it decreased the duration of both PTP and the Ca2+ -activated K+ current.