Action potentials must admit calcium to evoke transmitter release.
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.
Mulkey
R M
RM
Department of Molecular and Cell Biology, University of California, Berkekey 94720.
Zucker
R S
RS
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*
D015220:Calcium Channels; D018377:Neurotransmitter Agents; D002118:Calcium