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pubmed-article:9748528pubmed:abstractTextTissue levels of the endogenous excitatory amino acid receptor antagonist kynurenic acid (KYNA) and of its bioprecursor L-kynurenine were measured in rats of different ages after d-amphetamine administration. In adult animals, extracellular KYNA concentrations were also determined in vivo by hippocampal microdialysis. In the adult brain, d-amphetamine caused a transient, dose-dependent decrease in tissue content and extracellular levels of KYNA, reaching a nadir of approximately 70% of control values after 1 h at 5 mg/kg. Quantitatively similar decrements were observed in four different brain regions. Seven, 14 and 28-day-old pups were particularly sensitive to the drug, showing a reduction in forebrain KYNA levels to 25%, 40% and 35% of control values, respectively, 1 h after the administration of 5 mg/kg d-amphetamine. Notably, no changes in brain L-kynurenine levels and in liver L-kynurenine and KYNA concentrations were found after d-amphetamine administration. Thus, endogenous monoamines released by d-amphetamine may interfere with the transamination of L-kynurenine to KYNA specifically in the brain. These results suggest that d-amphetamine increases excitatory amino acid receptor function temporarily by reducing the levels of endogenous KYNA.lld:pubmed
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pubmed-article:9748528pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:9748528pubmed:articleTitleSystemic d-amphetamine administration causes a reduction of kynurenic acid levels in rat brain.lld:pubmed
pubmed-article:9748528pubmed:affiliationMaryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore 21228, USA.lld:pubmed
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pubmed-article:9748528pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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