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Titolo:
Excitotoxic injury stimulates pro-drug-induced 7-chlorokynurenate formation in the rat striatum in vivo
Autore:
Lee, SC; Schwarcz, R;
Indirizzi:
Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Baltimore, MD 21228 USAUniv Maryland Baltimore MD USA 21228 iat Res Ctr, Baltimore, MD 21228 USA
Titolo Testata:
NEUROSCIENCE LETTERS
fascicolo: 3, volume: 304, anno: 2001,
pagine: 185 - 188
SICI:
0304-3940(20010525)304:3<185:EISP7F>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
KYNURENIC ACID SYNTHESIS; NMDA RECEPTOR; IN-VIVO; BRAIN; GLYCINE; 4-CHLOROKYNURENINE; NEUROTOXICITY; HIPPOCAMPUS;
Keywords:
astrocytes; excitotoxicity; glia; kynurenines; neurodegeneration; neuroprotection; N-methyl-D-aspartate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Schwarcz, R Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, POB 21247, Baltimore, MD 21228 USA Univ Maryland POB 21247 Baltimore MD USA 21228 e, MD 21228 USA
Citazione:
S.C. Lee e R. Schwarcz, "Excitotoxic injury stimulates pro-drug-induced 7-chlorokynurenate formation in the rat striatum in vivo", NEUROSCI L, 304(3), 2001, pp. 185-188

Abstract

Peripheral administration of L-4-chlorokynurenine (4-Cl-KYN), which is enzymatically converted in astrocytes to form the glycine(B) receptor antagonist 7-chlorokynurenic acid (7-Cl-KYNA), has been shown to provide neuroprotection against excitotoxic damage. The present study was designed to examinethe metabolic fate of 4-Cl-KYN after systemic injection, and to study its brain uptake and subsequent transamination during the acute phase followingan excitotoxic insult. To this end, adult rats received intrastriatal injections of vehicle (1 mul) or quinolinic acid (QUIN) (240 nmol/l mul), and were administered 50 mg/kg 4-Cl-KYN (intraperitoneally) immediately after surgery. After 90 and 180 min, 7-Cl-KYNA concentrations in the vehicle-injected striatum were 54 +/- 13 and 16 +/- 2 nM, respectively. The contralateral, QUIN-injected striatum contained 212 +/- 39 and 97 +/- 27 nM 7-Cl-KYNA, respectively. This injury-induced increase was accompanied by slightly higher 4-Cl-KYN levels in the QUIN-treated striatum, indicating that better pro-drug availability in part accounts for the enhanced 7-Cl-KYNA formation. These data demonstrate that systemic 4-Cl-KYN application, by targeting reactive glial cells during the early, reversible stage of excitotoxic neurodegeneration, produces disproportionately large amounts of the neuroprotectant 7-Cl-KYNA at the site of the emerging lesion. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 19:13:43