Role of Stored Calcium in the Regulation of Neurotransmitter Quantum Size

• Published in: Bulletin of experimental biology and medicine 2012-02, Vol.152 (4), p.392-396
• Main Authors: Skiteva, O. I., Lapteva, V. I., Balezina, O. P.
• Format: Article
• Language: English
• Subjects: Acetylcholine; Acetylcholine - metabolism; Animals; Antagonists; Benzophenanthridines - pharmacology; Biomedical and Life Sciences; Biomedicine; Caffeine; Caffeine - pharmacology; Calcium (intracellular); Calcium - metabolism; Cations, Divalent; Cell Biology; chelerythrine; Cholinergic Antagonists - pharmacology; Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors; Cyclic AMP-Dependent Protein Kinases - metabolism; Egtazic Acid - analogs & derivatives; Egtazic Acid - pharmacology; Endplate potential; Internal Medicine; Ions; Isoquinolines - pharmacology; Laboratory Medicine; Mice; Miniature Postsynaptic Potentials - drug effects; Miniature Postsynaptic Potentials - physiology; Nerve endings; Neuromuscular Junction - drug effects; Neuromuscular Junction - physiology; Neurotransmitters; Pathology; Piperidines - pharmacology; Presynaptic Terminals - drug effects; Presynaptic Terminals - physiology; Protein kinase A; Protein kinase C; Protein Kinase C - antagonists & inhibitors; Protein Kinase C - metabolism; Ryanodine - pharmacology; Ryanodine Receptor Calcium Release Channel - metabolism; Ryanodine receptors; Sulfonamides - pharmacology; Tissue Culture Techniques; vesamicol; Vesicles
• ISSN: 0007-4888; 1573-8221
• DOI: 10.1007/s10517-012-1536-8

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.