Genetic dissection of short-term and long-term facilitation at the Drosophila neuromuscular junction.
Transmitter release at the Drosophila larval neuromuscular junction may be increased by previous activity of the nerve. This facilitation phenomenon involves at least two processes, one short-term and other long-term. These are shown to based on different mechanisms because (i) a mutant was found that had abnormal long-term facilitation but normal short-term  facilitation; and (ii) long-term facilitation was eliminated by tetrodotoxin or by removing external Na+ but short-term facilitation was not. In long-term facilitation, there was a prolonged release of transmitter due to a prolonged Ca2+ sensitivity of the presynaptic terminal after each nerve stimulus. The cause of this is probably accumulation of Na+ inside the nerve terminal.
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D004331:Drosophila melanogaster / Q000235:genetics; D007700:Kinetics; D008094:Lithium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009154:Mutation; D009469:Neuromuscular Junction / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects
D018377:Neurotransmitter Agents; D010042:Ouabain; D008094:Lithium; D012964:Sodium; D011188:Potassium; D002118:Calcium