Calcium ionophore X-537A increases spontaneous and phasic quantal release of acetylcholine at frog neuromuscular junction.

Abstract

TRANSMITTER release from nerve endings is believed to be triggered by the influx of Ca2+, which is thought to enter the terminal as a result of an increase in conductance produced by the action potential1. At the neuromuscular junction the evidence for the role of Ca2+ is largely indirect, based on changes in endplate potential (e.p.p.) amplitude following variations in [Ca2+]0. Miledi2 showed that microinjection of Ca2+ into the presynaptic terminal at the synapse of the squid giant axon causes a brief period of enhanced quantal release. Ca2+ also affects the rate of spontaneous quantal release at the neuromuscular junction; miniature end-plate potential (m.e.p.p.) frequencies are very low in solutions with reduced Ca2+ (ref. 3–5) The mode of action of Ca2+ within the terminal remains largely a matter of speculation. Now a new tool has become available: an ionophore, X-537A, that transfers both univalent and divalent cations across lipid bilayers and cell membranes6–10. Using X-537A it may be possible to change intracellular Ca2+ levels while observing changes in quantal release. The ionophore might also be used to transfer other divalent metal ions into the terminal, to see how effective they are compared with Ca2+.