Characterization of L-glutamate action on the release of endogenous dopamine from the rat caudate-putamen
In the present study the effect of L-glutamic acid (L-Glu), N-methyl-D-aspartic acid (NMDA), kainic acid (KA) and quisqualic acid (QUIS) on the release of endogenous dopamine (DA) from slices of the rat caudate-putamen was investigated. DA was measured by high-performance liquid chromatography coupl...
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Published in | The Journal of pharmacology and experimental therapeutics Vol. 248; no. 2; pp. 722 - 728 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
American Society for Pharmacology and Experimental Therapeutics
01.02.1989
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Subjects | |
Online Access | Get full text |
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Summary: | In the present study the effect of L-glutamic acid (L-Glu), N-methyl-D-aspartic acid (NMDA), kainic acid (KA) and quisqualic
acid (QUIS) on the release of endogenous dopamine (DA) from slices of the rat caudate-putamen was investigated. DA was measured
by high-performance liquid chromatography coupled to an electrochemical detector. L-Glu, NMDA, KA and QUIS, in the absence
of Mg++, produced a dose-related, Ca++-dependent increase in DA release. The order of agonist efficacy was L-Glu greater than
NMDA greater than KA = QUIS. D-2-amino-7-phosphonoheptanoic acid (0.5 mM), but not L-2-amino-7-phosphonoheptanoic acid, antagonized
the action of L-Glu and NMDA, but did not modify the effect of KA or QUIS. Tetrodotoxin (0.1 microM) partially inhibited the
stimulatory effect of KA and QUIS, but not that of L-Glu or NMDA. Mg++ (1.2 mM) abolished the excitatory effect of NMDA, significantly
reduced the action of L-Glu, but did not influence the action of KA or QUIS. The inhibitory action of Mg++ on the L-Glu-induced
DA release was reversed when L-Glu was coupled to high concentrations of K+. N-allylnormetazocine (SKF-10,047), a benzmorphan
agent, produced a stereospecific inhibition of L-Glu-induced DA release. This inhibition was also produced by 1-[1-(2-thienyl)cyclohexyl]piperidine,
a phencyclidine receptor ligand, but not by 1,3-di-O-tolylguanidine, a sigma receptor-selective ligand. The results of this
study show that L-Glu increases DA release predominantly by activation of the NMDA receptor located presynaptically on dopaminergic
afferents. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-3565 1521-0103 |