Calcium metabolism and acetylcholine release at the nerve-electroplaque junction.

1. Calcium metabolism was investigated in the electric organ of Torpedo at rest and during synaptic activity. When the tissue was incubated in high calcium concentrations, complete exchange was obtained between cellular calcium and that of the external medium. In the presence of low concentrations, the tissue retained its calcium which, in this case, was poorly exchanged. 2. Stimulation of the nerves to the electric organ provoked a net increase in cellular calcium and an acceleration of its exchange with that of the extracellular space. This entry of calcium seemed to involve mainly the presynaptic axon endings since it occurred even when transmission was blocked by curare. 3. The presynaptic accumulation of calcium was accompanied by a decrease in the vesicular pool of acetylcholine (ACh). On the other hand, the level of extracellular Ca2+ seemed to be critical for the intraterminal repartition of ACh between the vesicular pool and the cytoplasmic pool, and also for exchange of high energy phosphate between ATP and thiamine esters. 4. Radioautography of 45Ca at the electron microscope level confirmed that most of the Ca accumulation following stimulation concerned the presynaptic axon endings. The accumulated 45Ca was closely associated with the plasma-lemma region of nerve terminals, mainly in the region of active zones. 5. Taking this into account, and also the fact that synaptic vesicles have a very efficient Ca sequestration mechanism (see Israël et al., this symposium) it is proposed that, after entry, Ca is taken up by the vesicles situated in active zones, exchanged against vesicular ACh, concentrated in the vesicle and finally released by exocytosis.