Action potentials must admit calcium to evoke transmitter release

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  • A Correction to this article was published on 30 May 1991

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) doi:10.1038/350153a0

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