Abstract
Relatively high external Mg 2+ specifically induces a shoulder in the post-tetanic decay of miniature endplate potential frequency at frog neuromuscular junctions. This effect is antagonized by Ca 2+, but not by Sr 2+ and Mn 2+. This shoulder formation is not caused by Mn 2 or dinitrophenol in the medium. It is suggested that Mg 2+ enters nerve terminals and displaces Ca 2+ from internal stores; Mg 2+ subsequently interferes with Ca 2+ removal until the Mg 2+ itself has been removed. The dinitrophenol result suggests that ATP-dependent Ca 2+ extrusion is not permanently slowed. An equally likely and simpler explanation is that Mg 2+ enters nerve terminals and the Mg 2+ itself causes an increase in miniature endplate potential frequency. External Ca 2+ competes with Mg 2+ for channel entry and prevents this effect. The time course of the decay of miniature endplate potential frequency reflects the processes involved in Mg 2+ extrusion and/or uptake.
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