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Titolo:
TREATMENT WITH AN AMPA ANTAGONIST 12 HOURS FOLLOWING SEVERE NORMOTHERMIC FOREBRAIN ISCHEMIA PREVENTS CA1 NEURONAL INJURY
Autore:
LI H; BUCHAN AM;
Indirizzi:
UNIV OTTAWA,OTTAWA CIV HOSP,1053 CARLING AVE OTTAWA K1Y 4E9 ONTARIO CANADA UNIV OTTAWA,OTTAWA CIV HOSP,1053 CARLING AVE OTTAWA K1Y 4E9 ONTARIO CANADA
Titolo Testata:
Journal of cerebral blood flow and metabolism
fascicolo: 6, volume: 13, anno: 1993,
pagine: 933 - 939
SICI:
0271-678X(1993)13:6<933:TWAAA1>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTAMATE RECEPTOR CHANNELS; D-ASPARTATE ANTAGONIST; FOCAL ISCHEMIA; KAINATE RECEPTORS; CEREBRAL-ISCHEMIA; NMDA ANTAGONIST; GLOBAL-ISCHEMIA; CALCIUM-UPTAKE; GLIAL-CELLS; ADULT-RATS;
Keywords:
ALPHA-AMINO-3-HYDROXY-5-METHYL-4-ISOXAZOLE PROPIONATE ANTAGONISTS; CA1 HIPPOCAMPUS; CEREBRAL ISCHEMIA; EXCITOTOXICITY; N-METHYL-D-ASPARTATE ANTAGONISTS; RATS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
46
Recensione:
Indirizzi per estratti:
Citazione:
H. Li e A.M. Buchan, "TREATMENT WITH AN AMPA ANTAGONIST 12 HOURS FOLLOWING SEVERE NORMOTHERMIC FOREBRAIN ISCHEMIA PREVENTS CA1 NEURONAL INJURY", Journal of cerebral blood flow and metabolism, 13(6), 1993, pp. 933-939

Abstract

The neuroprotective effects of 3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (NBQX). GYKI 52466, and MK-801 were tested following severe forebrain ischemia. Wistar rats were subjected to 10 min of normothermic ischemia and reperfused for 7 days. Necrotic hippocampal CA1 neurons were counted and expressed as a percentage (mean +/- SD). In Experiment 1, saline-treated rats sustained 81 +/- 20% damage to dorsal CA1. Rats given NBQX 30 mg/kg i.p. x3 lost 21 +/- 27% (p < 0.01). Neither MK-801 1 mg i.p. x3 alone, nor in combination with the cytoprotective dose of NBQX protected CA1, with 83 +/- 18 and 54 +/- 34% damage. respectively (NS). Giving NBQX 90 mg/kg i.v. did not protect cells (94 +/- 5%) and resulted in nephrotoxicity. In Experiment 2, rats were given saline or three doses of NBQX 30 mg/kg i.p. immediately at reperfusion (RP) or after a 6-, 12-, or 24-h delay. Saline-treated rats suffered 79 +/- 16% injury. NBQX given immediately resulted in 17 +/- 17% injury, and even if treatment was delayed by either 6 or 12 h, there was marked protection with only 27 +/- 32 and 25 +/- 17% injury, respectively (all p < 0.01). Delaying the initiation of treatment to 24 h was not successful, resulting in 50 +/- 28% injury (NS). In Experiment 3, saline-treated rats lost 81 +/- 19% of CA1 cells, while those given GYKI 52466 10 mg/kg i.p. x5 starting immediately following RP lost 80 +/-14%. Blocking alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors with NBQX postischemia is highly efficacious, indicating that delayed degeneration of CA1 cells is AMPA rather than N-methyl-D-aspartate (NMDA) receptor-linked and is reversible for CA1 cells for at least 12 h.

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Documento generato il 21/09/20 alle ore 05:34:16