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.
Narita
K
K
Department of Physiology, Kawasaki Medical School, Okayama, Japan.
Kita
H
H
D019297:2,4-Dinitrophenol; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001693:Biological Transport, Active; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002413:Cations, Divalent / Q000494:pharmacology*; D004140:Dinitrophenols / Q000494:pharmacology; D004347:Drug Interactions; D009045:Motor Endplate / Q000187:drug effects* / Q000502:physiology; D011898:Ranidae; D013746:Tetany / Q000378:metabolism*
D002413:Cations, Divalent; D004140:Dinitrophenols; D000252:Calcium-Transporting ATPases; D019297:2,4-Dinitrophenol