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.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001048:Aplysia; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology*; D004533:Egtazic Acid / Q000494:pharmacology; D005724:Ganglia / Q000187:drug effects / Q000502:physiology; D007473:Ion Channels / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
D007473:Ion Channels; D013779:Tetrodotoxin; D004533:Egtazic Acid; D011188:Potassium; D002118:Calcium