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| Research article summary (published 12 Mar 1994): |
N-methyl-D-aspartate receptors modulate extracellular 5-hydroxytryptamine concentration in rat hippocampus and striatum in vivo.
Full Abstract
The effects of infusing N-methyl-D-aspartate (NMDA) and the specific NMDA receptor antagonist D-2-amino-5-phosphonopropionic acid (D-AP5) into rat hippocampus and striatum on extracellular 5-hydroxytryptamine (5-HT) and its metabolite 5-hydroxy-indoleacetic acid (5-HIAA) were studied using intracerebral microdialysis. In striatum, NMDA (1-100 microM) caused a concentration-dependent increase in 5-HT. D-AP5 (10 microM) infusion caused increased extracellular 5-HT. When the two drugs were co-infused, no effect on extracellular 5-HT was seen. D-AP5 alone was found to cause a delayed but sustained increase in dialysate 5-HIAA. In hippocampus, NMDA infusion caused a dose-dependent decrease in extracellular 5-HT while D-AP5 produced a transitory increase in 5-HT level. NMDA caused a decrease in dialysate 5-HIAA. In striatum, the effect of 10 microM NMDA infusion was abolished by co-infusion with tetrodotoxin (TTX; 1 microM). In hippocampus, 1 microM TTX caused a slight but non-significant augmentation of the effect of 10 microM NMDA alone. These data indicate that NMDA receptors mediate control over 5-HT release and metabolism in different brain regions and may in part explain the behavioural effects of non-competitive NMDA receptor antagonists.
Author information
Author/s: Whitton, P S (PS); Richards, D A (DA); Biggs, C S (CS); Fowler, L J (LJ);
Affiliation: Department of Pharmacology, School of Pharmacy, London, UK.
Journal and publication information
Publication Type: Journal Article
Journal: Neuroscience letters (Neurosci Lett), published in IRELAND. (Language: eng)
Reference: 1994-Mar; vol 169 (issue 1-2) : pp 215-8
Dates: Created 1994/09/01; Completed 1994/09/01; Revised 2003/11/14;
PMID: 7519338, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: 18 Feb 2009 00:00:00)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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