Abstract
To investigate whether any specific requirement for extracellular Ca2+ exists in the control synaptic vesicle retrieval, we examined the ability of the divalent cation Ba2+ to substitute for Ca2+ in both vesicle exocytosis and endocytosis. Ba2+ stimulated glutamate release from rat cerebrocortical synaptosomes. Ba2+-evoked release was inhibited by bafilomycin A1, indicating release was via exocytosis of synaptic vesicles. However, Ba2+ did not stimulate vesicle retrieval, monitored by a FM2-10-based retrieval assay. Therefore synaptic vesicle retrieval in central nerve terminals has a specific requirement for extracellular Ca2+ and the Ca2+ receptor for retrieval has a different cation specificity to the Ca2+ receptor for exocytosis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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4-Aminopyridine / pharmacology
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Animals
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Anti-Bacterial Agents / pharmacology
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Barium / pharmacology*
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Cations, Divalent / pharmacology
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Cerebral Cortex / physiology*
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Endocytosis / drug effects
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Enzyme Inhibitors / pharmacology
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Exocytosis / drug effects
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Fluorescent Dyes
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Glutamic Acid / metabolism
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Macrolides*
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Potassium Chloride / pharmacology
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Proton-Translocating ATPases / antagonists & inhibitors
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Pyridinium Compounds
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Quaternary Ammonium Compounds
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Rats
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Rats, Sprague-Dawley
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Synaptic Vesicles / drug effects
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Synaptic Vesicles / physiology*
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Synaptosomes / drug effects
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Synaptosomes / physiology*
Substances
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Anti-Bacterial Agents
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Cations, Divalent
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Enzyme Inhibitors
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FM2 10
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Fluorescent Dyes
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Macrolides
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Pyridinium Compounds
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Quaternary Ammonium Compounds
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Barium
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Glutamic Acid
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Potassium Chloride
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bafilomycin A1
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4-Aminopyridine
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Proton-Translocating ATPases