ryanodine and vesamicol

Release of stored calcium ions during activation of ryanodine receptors with ryanodine or caffeine elevates the mean amplitude of spontaneous miniature end-plate potentials. Blockade of these receptors with selective antagonists abolishes this effect. Preliminary loading of the motor nerve terminals with intracellular calcium buffer EGTA-AM, but not with BAPTA-AM, also completely prevented the ryanodine-induced increment of miniature end-plate potential amplitude probably induced by the release of stored calcium. Vesamicol, a selective blocker of acetylcholine transport into vesicles, prevented the ryanodine-induced increment of the mean amplitude of miniature end-plate potentials. This increment was 2-fold more pronounced after preliminary blockade of protein kinase C with chelerythrine and was completely abolished by blockade of protein kinase A with H-89.

Topics: Acetylcholine; Animals; Benzophenanthridines; Caffeine; Calcium; Cations, Divalent; Cholinergic Antagonists; Cyclic AMP-Dependent Protein Kinases; Egtazic Acid; Isoquinolines; Mice; Miniature Postsynaptic Potentials; Neuromuscular Junction; Piperidines; Presynaptic Terminals; Protein Kinase C; Ryanodine; Ryanodine Receptor Calcium Release Channel; Sulfonamides; Tissue Culture Techniques