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Characterization of the Exocytotic Release of Glutamate from Guinea‐Pig Cerebral Cortical Synaptosomes
Author(s) -
SanchezPrieto Jose,
Sihra Talvinder S.,
Nicholls David G.
Publication year - 1987
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1987.tb03394.x
Subject(s) - guinea pig , glutamate receptor , neuroscience , cerebral cortex , synaptosome , chemistry , excitatory amino acid transporter , biology , biochemistry , endocrinology , central nervous system , receptor
A continuous enzyme‐linked fluorometric assay was used for determining the characteristics for glutamate exocytosis from guinea‐pig cerebrocortical synaptosomes. Ca 2+ ‐dependent release can be induced not only by K + , but also by the Na + channel activator veratridine and the Ca 2+ ionophore ionomycin. K + ‐induced release can be inhibited by the Ca 2+ channel inhibitor verapamil. Sr 2+ and Ba 2+ substitute for Ca 2+ in promoting K + ‐induced release. Agents that would be predicted to transform the transvesicular pH gradient into a membrane potential are without effect on glutamate release. However, the protonophore carbonylcy‐anide p ‐trifluoromethoxyphenylhydrazone causes a time‐dependent loss of exocytosis that is oligomycin insensitive and may be due to depletion of vesicular glutamate. The Ca 2+ ‐independent release of glutamate from the cytosol on depolarization is unchanged or promoted by metabolic inhibitors that lower the ATP/ADP ratio. In contrast, Ca 2+ ‐dependent release is ATP dependent and is blocked by the combined inhibition of oxidative phosphorylation and glycolysis.