| Literature DB >> 10721048 |
R Schwarcz1, G Ceresoli-Borroni, H Q Wu, A Rassoulpour, B Poeggeler, P S Hodgkins, P Guidetti.
Abstract
Using in vivo and in vitro paradigms, the regulation and function of the brain metabolite kynurenic acid (KYNA) was examined in rats on postnatal days (PND) 7 and 14. As shown previously in adult rats, glucose removal and d-amphetamine (d-Amph) administration caused decreases in KYNA formation, while exposure to pyruvate up-regulated KYNA synthesis. The effect of glucose deprivation was substantially blunted in immature animals. In PND 14 rats, d-Amph pre-treatment exacerbated the excitotoxic effects of an intrastriatal N-methyl-D-aspartate (NMDA) injection. This potentiation was prevented by m-nitrobenzoylalanine, a kynurenine 3-hydroxylase inhibitor that also antagonized the KYNA reduction caused by d-Amph. These and additional experiments with the competitive NMDA receptor antagonist CGP 40116 indicate the existence of a functionally significant, novel high-affinity receptor for KYNA in the brain.Entities:
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Year: 1999 PMID： 10721048 DOI： 10.1007/978-1-4615-4709-9_17
Source DB: PubMed Journal: Adv Exp Med Biol ISSN： 0065-2598 Impact factor: 2.622