作者
Melvyn P HEYES, K Saito, JS Crowley, LE Davis, MA Demitrack, M Der, LA Dilling, J Elia, MJP Kruesi, A Lackner, SA Larsen, K Lee, HL Leonard, SP Markey, A Martin, S Milstein, MM Mouradian, MR Pranzatelli, BJ Quearry, A Salazar, M Smith, SE Strauss, T Sunderland, SW Swedo, WW Tourtellotte
发表日期
1992/10/1
期刊
Brain
卷号
115
期号
5
页码范围
1249-1273
出版商
Oxford University Press
简介
Neurological dysfunction, seizures and brain atrophy occur in a broad spectrum of acute and chronic neurological diseases. In certain instances, over-stimulation of N-methyl-D-aspartate receptors has been implicated Quinolinic acid (QUIN) is an endogenous N-methyl-D-aspartate receptor agonist synthesized from L-tryptophan via the kynurenine pathway and thereby has the potential of mediating N-methyl-D-aspartate neuronal damage and dysfunction. Conversely, the related metabolite, kynurenic acid, is an antagonist of N-methyl-D-aspartate receptors and could modulate the neurotoxic effects of QUIN as well as disrupt excitatory amino acid neurotransmission In the present study, markedly increased concentrations of QUIN were found in both lumbar cerebrospinal fluid (CSF) and post-mortem brain tissue of patients with inflammatory diseases (bacterial, viral, fungal and parasitic infections, meningitis …
引用总数
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