Calcium-dependent release of accumulated glutamate from synaptic vesicles within permeabilized nerve terminals.
We have studied glutamate release from synaptic vesicles in permeabilized synaptosomes, which were preloaded with [3H]glutamate in an ATP-dependent manner. The release was found to be calcium-dependent and to require a heat-labile cytosolic macromolecule factor for maximum activity. Maximal release occurred at 5 microM free Ca2+ and within 5 min. Of the other divalent cations tested, only barium stimulated release of vesicular glutamate. The release was inhibited by N-ethylmaleimide. These results are characteristic of exocytotic release of monoamines and peptides observed in endocrine systems, and constitute direct evidence for the notion that calcium-dependent release of glutamate originates from the vesicular pool.
Kish
P E
PE
Mental Health Research Institute, University of Michigan, Ann Arbor 48109.
Ueda
T
T
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000494:pharmacology*; D002413:Cations, Divalent; D004533:Egtazic Acid / Q000494:pharmacology; D005971:Glutamates / Q000378:metabolism*; D007700:Kinetics; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism*; D010539:Permeability; D051381:Rats; D013572:Synaptic Vesicles / Q000187:drug effects / Q000378:metabolism*; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism*
D002413:Cations, Divalent; D005971:Glutamates; D004533:Egtazic Acid; D000255:Adenosine Triphosphate; D002118:Calcium