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pubmed-article:1650394pubmed:abstractTextThe wide-ranging neuronal actions of glutamate are thought to be mediated by postsynaptic N-methyl-D-aspartate (NMDA) and non-NMDA receptors. The present report demonstrates the existence of presynaptic glutamate receptors in isolated striatal dopaminergic nerve terminals (synaptosomes). Activation of these receptors, by NMDA in the absence of Mg2+ and presence of glycine and by non-NMDA agonists in the presence of Mg2+, results in Ca(2+)-dependent release of dopamine from striatal synaptosomes. The release stimulated by NMDA is blocked by Mg2+ and by selective NMDA antagonists, whereas the release stimulated by selective non-NMDA agonists is blocked by a non-NMDA antagonist but not by Mg2+ or NMDA antagonists. Thus, these presynaptic glutamate receptors, localized on dopaminergic terminals in the striatum, appear to be pharmacologically similar to both the NMDA and the non-NMDA postsynaptic receptors. By modulating the release of dopamine, these presynaptic receptors may play an important role in transmitter interactions in the striatum.lld:pubmed
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pubmed-article:1650394pubmed:authorpubmed-author:WangJ KJKlld:pubmed
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pubmed-article:1650394pubmed:articleTitlePresynaptic glutamate receptors modulate dopamine release from striatal synaptosomes.lld:pubmed
pubmed-article:1650394pubmed:affiliationProgram in Neurosciences, Tufts University School of Medicine, Boston, Massachusetts 02111.lld:pubmed
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pubmed-article:1650394pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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