Tryptamine enhancement of neurotransmitter release under conditions that normally depress calcium influx.
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 Ca2+-high Mg2+ media that depress Ca2+ influx. This suggests that in the presence of tryptamine, intracellular Ca2+ sources may support evoked, phasic neurotransmitter release.
Friedman
R N
RN
Shank
R P
RP
Freeman
A R
AR
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D008121:Nephropidae; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects*; D014363:Tryptamines / Q000494:pharmacology*
D018377:Neurotransmitter Agents; D014363:Tryptamines; C030820:tryptamine; D002118:Calcium