On the conductance pathway traversed by strontium in mediating the asynchronous release of acetylcholine by motor nerve impulses.
A study was made to determine whether the Sr2+ dependent asynchronous release of acetylcholine by nerve impulses is mediated by the conventional Ca2+ conductance channel or, as has been suggested recently, through an alternative ion pathway. Experiments were performed on the frog neuromuscular junction by the use of standard electrophysiological techniques. Repetitive nerve stimulation in Sr2+-Ringer solutions caused a marked increase in miniature end-plate potential (m.e.p.p.) frequency which was dependent on Sr2+ concentration and inhibited in a competitive fashion by the known Ca2+ antagonists, Co2+ and Mg2+. The equilibrium dissociation constants (KdS) determined for both Co2+ (0.09 +/- 0.01 mM, mean +/- s.e. mean, n = 5) and Mg2+ (3.7 +/- 0.3 mM, mean +/- s.e. mean, n = 4) were essentially the same as the reported values for these antagonists in blocking Ca2+ -mediated transmitter release by nerve impulses. These results suggest that Sr2+ mediates asynchronous evoked transmitter release through the conventional calcium conductance channel.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001001:Anura; D003035:Cobalt / Q000494:pharmacology; D066298:In Vitro Techniques; D008274:Magnesium / Q000494:pharmacology; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism*; D009431:Neural Conduction / Q000187:drug effects*; D009469:Neuromuscular Junction / Q000187:drug effects; D013324:Strontium / Q000037:antagonists & inhibitors / Q000494:pharmacology*
D003035:Cobalt; D008274:Magnesium; D000109:Acetylcholine; D013324:Strontium