Journal article
Rapid chelation of calcium entering isolated rat brain nerve terminals during stimulation inhibits neurotransmitter release
Neuroscience letters, v 211(2)
1996
PMID: 8830863
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The intracellular actions of calcium chelators on the release of the neurotransmitter glutamate from isolated rat brain nerve terminals (synaptosomes) were examined. Preloading synaptosomes with the rapid calcium-binding chelator 1,2-bis(2-aminophenoxy)ethane-
N,N,N′,N′- tetraacetic acid (BAPTA) resulted in a decrease in K
+-stimulated glutamate release to nearly half that of controls, whereas preloading with the calcium chelator EGTA, whose action is less rapid than that of BAPTA, was without effect. Inhibition of glutamate release was also observed on preloading synaptosomes with dibromo-BAPTA, but not with dinitro-BAPTA. K
+-stimulated, Ca
2+-dependent synaptosomal protein phosphorylation was not affected after preloading with BAPTA. The results suggest that the calcium-dependent intracellular component essential for triggering the secretory response in mammalian brain nerve terminals resides near the calcium channels, binding; calcium rapidly on its entry during stimulation.
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Details
- Title
- Rapid chelation of calcium entering isolated rat brain nerve terminals during stimulation inhibits neurotransmitter release
- Creators
- Robert A. Nichols - Drexel UniversityGregory R. Suplick - Drexel University
- Publication Details
- Neuroscience letters, v 211(2)
- Publisher
- Elsevier Ireland Ltd
- Resource Type
- Journal article
- Language
- English
- Web of Science ID
- WOS:A1996UV61500017
- Scopus ID
- 2-s2.0-0030596540
- Other Identifier
- 991019350583104721
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- Web of Science research areas
- Neurosciences