The effect of calcium ions on the binomial parameters that control acetylcholine release during trains of nerve impulses at amphibian neuromuscular synapses

Abstract

A study was made of the effects of changing the external calcium concentration [Ca]o on the binomial parameters p and n that control the average quantal content (.hivin.m) of the end-plate potential (epp) during trains of nerve impulses at synapses in amphibian [Bufo marinus] striated muscle. In high external Ca concentrations (0.4 mM .ltoreq. [Ca]o < 1.0 mM) the increase in .hivin.m of a test impulse following a conditioning impulse at different intervals (< 100 ms) was due to an increase in the number of quanta available for release, n; the increase in .hivin.m of successive epp in a short high frequency train was primarily due to an increase in n. In high external Ca concentrations (1.0 mM .ltoreq. [Ca]o < 10 mM) there was a decrease in .hivin.m of a test impulse following a short high frequency conditioning train (4-5 impulses, 20-100 Hz) at different intervals (200 ms < interval < 5 s) and this was due to a decrease in the number of quanta available for release, n; in a long high frequency train (20 impulses, 20-100 Hz) there was an increase in .hivin.m for the first few successive epp followed by a depression of .hivin.m which eventually reached a steady state and these changes in .hivin.m were due to changes in n; the higher the frequency the greater was the depression in n during the steady-state period. In high Ca concentrations, the steady-state .hivin.m reached in the first 20 impulses during continual stimulation at high frequency gave way to a decline in .hivin.m over several minutes until a new depressed steady-state value of .hivin.m was reached and this was maintained during the longest periods of stimulation (30 min); this decline in .hivin.m was primarily due to a decline in the number of quanta available for release. These changes in the number of quanta available for release during trains of impulses are predicted in terms of a hypothesis in which facilitation is due to the accumulation of a residual Ca-receptor complex in the nerve terminal that determines the fraction of a pool of quanta which contributes to n, and depression is due to a decrease in the number of quanta in this pool.