STRONTIUM AND QUANTAL RELEASE OF TRANSMITTER AT NEUROMUSCULAR JUNCTION

1. Previous work has shown that in calcium‐free solutions nerve impulses invade the motor nerve terminals at the neuromuscular junction, but fail to release transmitter. In these conditions, strontium ions applied iontophoretically to a minute part of a junction, or to the whole muscle by bath application, restore to the nerve impulse its ability to release transmitter. 2. As with calcium, the transmitter released in the presence of strontium is in the form of packages (quanta) whose release can be predicted from Poisson's Theorem. 3. The mean number of quanta released by a nerve impulse increases with the concentration of strontium. Strontium is much less effective than calcium in equimolar concentrations. 4. Transmitter quanta released in the presence of strontium evoke larger unit potentials than quanta released in the presence of calcium. The larger size of the Sr‐unit potentials is caused by a prolongation of transmitter action, presumably due to a post‐synaptic effect of strontium. 5. Neuromuscular transmission was blocked in some fibres when the concentration of strontium was raised beyond 10 m M. This junctional block was presumably due to a failure in the propagation of nerve impulses. 6. The post‐stimulation increase in the frequency of miniature end‐plate potentials, which is normally seen in calcium solutions, is also observed when calcium is substituted by strontium. The post‐stimulation effect increases with the concentration of strontium. 7. It is concluded that strontium can substitute for calcium in the process of quantal release of transmitter. The physico‐chemical mechanism of this substitution remains unknown. © 1969 The Physiological Society