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Titolo:
PRETREATMENT BUT NOT POSTTREATMENT WITH GYKI-52466 REDUCES FUNCTIONALDEFICITS AND NEURONAL DAMAGE AFTER GLOBAL-ISCHEMIA IN RATS
Autore:
BLOCK F; SCHMITT W; SCHWARZ M;
Indirizzi:
RHEIN WESTFAL TH AACHEN,DEPT NEUROL,PAUWELSSTR 30 D-52057 AACHEN GERMANY
Titolo Testata:
Journal of the neurological sciences
fascicolo: 2, volume: 139, anno: 1996,
pagine: 167 - 172
SICI:
0022-510X(1996)139:2<167:PBNPWG>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSIENT FOREBRAIN ISCHEMIA; NON-NMDA ANTAGONISTS; CEREBRAL-ISCHEMIA; BRAIN-DAMAGE; SELECTIVE VULNERABILITY; GERBIL MODEL; WATER MAZE; HIPPOCAMPUS; CA1; GYKI-52466;
Keywords:
BEHAVIOR; CEREBRAL ISCHEMIA; GLUTAMATE; GYKI 52466; RAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
F. Block et al., "PRETREATMENT BUT NOT POSTTREATMENT WITH GYKI-52466 REDUCES FUNCTIONALDEFICITS AND NEURONAL DAMAGE AFTER GLOBAL-ISCHEMIA IN RATS", Journal of the neurological sciences, 139(2), 1996, pp. 167-172

Abstract

Glutamate antagonists have been shown to be neuroprotective in animalmodels of cerebral ischemia. Global cerebral ischemia in rats leads to selective neuronal damage in the hippocampus and striatum. Followingischemia a deficit in spatial learning and memory occurs. The aim of the present study was to investigate the potential neuroprotective effect of GYKI 52466, an antagonist at the non-N-methyl-D-aspartate receptor, with behavioural and histological measures of global ischemia in rats. Global ischemia was induced by four-vessel-occlusion (4VO) for 20 min in rats. GYKI 52466 (30 mg/kg i.p.) was administered either 20 min before induction of ischemia or immediately after onset of reperfusion. One week after surgery spatial learning was tested in the Morris water maze. After behavioural testing the animals were sacrificed and the neuronal damaged was assessed. GYKI 52466 reduced the increase in escape latency and in swim distance induced by 4VO when given before ischemia but not when applied after ischemia. Neuronal damage in the CA1 sector of the hippocampus produced by 4VO was significantly attenuated by pretreatment but not by posttreatment with GYKI 52466. Striatal neuronal damage was not affected by either treatment with GYKI 52466. GYKI 52466 had neuroprotective effects in a rat model of global cerebral ischemia. Pretreatment with GYKI 52466 protected rats against behavioural deficits and hippocampal neuronal damage induced by 4VO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 14:14:10