Abstract
THERE are two hypotheses to explain how neurons release transmitter. The calcium hypothesis proposes that membrane depolarization is necessary only for opening calcium channels and increasing internal calcium concentration ([Ca2+]i) near membrane transmitter-release sites1–3. These calcium ions trigger a transient release of neurotransmitter4,5. The calcium-voltage hypothesis postulates that voltage induces a conformational change in a membrane protein rendering it sensitive to calcium such that, in the presence of high [Ca2+]i depolarization directly triggers transmitter release6–9. Here we report that when calcium influx is blocked by cobalt or manganese ions in a calcium-free Ringer, as measured with Fura-2, and [Ca2+]i is elevated by liberation from a caged calcium compound, transmitter release at the crayfish neuromuscular junction is unaffected by presynaptic action potentials. These results support the calcium hypothesis.
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Mulkey, R., Zucker, R. Action potentials must admit calcium to evoke transmitter release. Nature 350, 153–155 (1991). https://doi.org/10.1038/350153a0
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DOI: https://doi.org/10.1038/350153a0
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