Abstract
Neurotransmitter release, resulting in excitatory and inhibitory junction potentials (E- and IJPs) is normally mediated by an influx of calcium ions into nerve terminals following depolarization. At a lobster neuromuscular junction, tryptamine is shown to greatly enhance the amplitude and duration of evoked E- and IJPs in low Ca 2+-high Mg 2+ media that depress Ca 2+ influx. This suggests that in the presence of tryptamine, intracellular Ca 2+ sources may support evoked, phasic neurotransmitter release.
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