The role of calcium ions in tetanic and post‐tetanic increase of miniature end‐plate potential frequency.

Abstract

The role of Ca2+ in transmitter release changes, during and after high frequency stimulation of the motor nerve (10-100 Hz), was examined at the frog neuromuscular junction. The stimulation-induced changes in miniature end-plate potential frequency (f) resembled the changes in end-plate potential amplitude recently described by Magleby and Zengel. The effects of tetanic stimulation on f under inward electrochemical gradient for Ca2+ were compared with those under reversed gradient and 4 differences were found: the increase in f during the tetanus under reversed Ca gradient conditions is much smaller than with an inward Ca gradient; the increase in f under reversed Ca gradient is preceded by a small decrease in f, whereas with an inward Ca gradient an immediate increase in f is observed; after the termination of the tetanus with a reversed Ca gradient, there is a further increase in f, compared to a decrease with an inward Ca gradient; and the augmentation phase of post-tetanic potentiation was practically abolished. The experimental results are explained by assuming that high frequency nerve stimulation causes an increase in transmitter release by at least 2 distinct processes: influx of Ca2+ through the presynaptic membrane and release of Ca2+ from intracellular stores. Na+ couple nerve activity to intracellular release of Ca.