Regulatory role of intracellular sodium ions in neurotransmitter secretion.
Calcium ions are the main inducer of quantal transmitter release of the frog neuromuscular junction; but even in their virtual absence from the extracellular medium, nerve stimulation causes a prolonged augmentation of transmitter release. These facts led to the hypothesis that an accumulation of intracellular sodium can serve as a slow secondary regulator of neurosecretion. Three lines of evidence presented in this article substantiate this hypothesis: firstly, veratridine, which is known to increase sodium fluxes through the voltage-dependent sodium channels, increases transmitter release after nerve stimulation. Secondly, monensin, which was shown to induce sodium transport through nerve membranes, increases evoked transmitter release, tetanic potentiation and posttetanic potentiation. Thirdly, sodium-filled phosphatidylcholine liposomes increase transmitter release. These effects of sodium are probably not due to a direct effect on the transmitter release mechanism, but are caused by sodium-induced calcium translocation from intracellular stores.
D000818:Animals; D066298:In Vitro Techniques; D008985:Monensin / Q000494:pharmacology; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011894:Rana pipiens; D011895:Rana ridibunda; D012964:Sodium / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects; D014701:Veratridine / Q000494:pharmacology
D018377:Neurotransmitter Agents; D014701:Veratridine; D008985:Monensin; D012964:Sodium