Post-tetanic potentiation of acetylcholine release at the frog neuromuscular junction develops after stimulation in Ca2+-free solutions.

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Abstract
At many synapses, previous activity increases the amount of transmitter released by a single action potential. This potentiation of transmitter release is usually attributed to the local accumulation of the Ca2+ that cross the axolemma during an action potential. Potentiated transmitter release can be observed at frog neuromuscular junctions after periods of repetitive stimulation in Ca2+-free solutions if Ca2+ is restored after the tetanus. The greater and more prolonged potentiation is, the lower the level of extracellular K+. This component of potentiation may be due to Ca2+ that accumulates within the terminal in exchange for intracellular Na+.