Effects of divalent cations on the time course of post-tetanic decay of miniature endplate potential frequency in frogs.

Relatively high external Mg2+ specifically induces a shoulder in the post-tetanic decay of miniature endplate potential frequency at frog neuromuscular junctions. This effect is antagonized by Ca2+, but not by Sr2+ and Mn2+. This shoulder formation is not caused by Mn2+ or dinitrophenol in the medium. It is suggested that Mg2+ enters nerve terminals and displaces Ca2+ from internal stores; Mg2+ subsequently interferes with Ca2+ removal until the Mg2+ itself has been removed. The dinitrophenol result suggests that ATP-dependent Ca2+ extrusion is not permanently slowed. An equally likely and simpler explanation is that Mg2+ enters nerve terminals and the Mg2+ itself causes an increase in miniature endplate potential frequency. External Ca2+ competes with Mg2+ for channel entry and prevents this effect. The time course of the decay of miniature endplate potential frequency reflects the processes involved in Mg2+ extrusion and/or uptake.