Post-tetanic potentiation of acetylcholine release at the frog neuromuscular junction develops after stimulation in Ca2+-free solutions.
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 calcium ions that cross the axolemma during an action potential. We found that 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. Potentiation is greater and more prolonged, 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+.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000502:physiology*; D005110:Extracellular Space / Q000502:physiology; D008274:Magnesium / Q000494:pharmacology; D009469:Neuromuscular Junction / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D011894:Rana pipiens; D012964:Sodium / Q000502:physiology; D009435:Synaptic Transmission
D012964:Sodium; D008274:Magnesium; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium