Abstract
Complete or partial replacement of Na+ by Li+ resulted in a progressively developing increase in the amplitude and quantal content of end-plate potentials of the frog neuromuscular junction. Analysis of frequency facilitation curves and estimations of the binomial parameters of release indicate that Li+ caused an increase in the probability of transmitter release. Li+ also caused a time dependent increase in the frequency of miniature end-plate potentials. The responsiveness of the miniature end-plate potentials to Li+ was depressed by elevated Ca++ and enhanced by elevated K+. Collectively, the effects of Li+ on transmitter release can be attributed to the accumulation by the nerve terminals of Li+ resulting on an increased level of intracellular Ca++.
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