Synaptic transmission and intracellular sodium: ionophore induced sodium loading of nerve terminals.
Application of the sodium ionophore, Monensin, to crustacean neuromuscular preparations induced a potentiation of the synaptic potential which subsided after removal of Monensin. The rate and extent of potentiation were influenced by the concentration of extracellular sodium, and potentiation occurred when Monensin was applied in calcium-free solutions. Some features of long-lasting facilitation induced by repetitive stimulation of the motor axon were duplicated by Monensin application. The results support the hypothesis that long-lasting facilitation of transmitter release can result from increased intracellular sodium.
D000818:Animals; D003400:Astacoidea; D003386:Brachyura; D002118:Calcium / Q000502:physiology; D004558:Electric Stimulation; D005663:Furans / Q000494:pharmacology*; D008985:Monensin / Q000494:pharmacology*; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D012964:Sodium / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects
D005663:Furans; D008985:Monensin; D012964:Sodium; D002118:Calcium