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Characterization of the Exocytotic Release of Glutamate from Guinea‐Pig Cerebral Cortical Synaptosomes

Characterization of the Exocytotic Release of Glutamate from Guinea‐Pig Cerebral Cortical... Abstract: A continuous enzyme‐linked fluorometric assay was used for determining the characteristics for glutamate exocytosis from guinea‐pig cerebrocortical synaptosomes. Ca2+‐dependent release can be induced not only by K+, but also by the Na+ channel activator veratridine and the Ca2+ ionophore ionomycin. K+‐induced release can be inhibited by the Ca2+ channel inhibitor verapamil. Sr2+ and Ba2+ substitute for Ca2+ 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 Ca2+‐independent release of glutamate from the cytosol on depolarization is unchanged or promoted by metabolic inhibitors that lower the ATP/ADP ratio. In contrast, Ca2+‐dependent release is ATP dependent and is blocked by the combined inhibition of oxidative phosphorylation and glycolysis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

Characterization of the Exocytotic Release of Glutamate from Guinea‐Pig Cerebral Cortical Synaptosomes

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References (41)

Publisher
Wiley
Copyright
Copyright © 1987 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3042
eISSN
1471-4159
DOI
10.1111/j.1471-4159.1987.tb03394.x
Publisher site
See Article on Publisher Site

Abstract

Abstract: A continuous enzyme‐linked fluorometric assay was used for determining the characteristics for glutamate exocytosis from guinea‐pig cerebrocortical synaptosomes. Ca2+‐dependent release can be induced not only by K+, but also by the Na+ channel activator veratridine and the Ca2+ ionophore ionomycin. K+‐induced release can be inhibited by the Ca2+ channel inhibitor verapamil. Sr2+ and Ba2+ substitute for Ca2+ 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 Ca2+‐independent release of glutamate from the cytosol on depolarization is unchanged or promoted by metabolic inhibitors that lower the ATP/ADP ratio. In contrast, Ca2+‐dependent release is ATP dependent and is blocked by the combined inhibition of oxidative phosphorylation and glycolysis.

Journal

Journal of NeurochemistryWiley

Published: Jul 1, 1987

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