title: Action potentials must admit calcium to evoke transmitter release.
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 sites. These calcium ions trigger a transient release of neurotransmitter. 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 release. 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.
authors.affiliation: Department of Molecular and Cell Biology, University of California, Berkekey 94720.
authors.forename: R M
authors.initials: RM
authors.lastname: Mulkey
authors.forename: R S
authors.initials: RS
authors.lastname: Zucker
mesh_terms: D000200:Action Potentials; D000818:Animals; D003400:Astacoidea; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology; D004558:Electric Stimulation; D008564:Membrane Potentials; D009469:Neuromuscular Junction / Q000378:metabolism / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism*
chemical_list: D015220:Calcium Channels; D018377:Neurotransmitter Agents; D002118:Calcium