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Titolo:
RESEARCH REPORT BETWEEN EXCITOTOXINS AND THE NA+ K+-ATPASE INHIBITOR OUABAIN IN CAUSING NEURONAL LESIONS IN THE RAT HIPPOCAMPUS/
Autore:
LEES GJ; LEONG W;
Indirizzi:
UNIV AUCKLAND,SCH MED,DEPT PSYCHIAT & BEHAV SCI AUCKLAND NEW ZEALAND
Titolo Testata:
Brain research
fascicolo: 1-2, volume: 714, anno: 1996,
pagine: 145 - 155
SICI:
0006-8993(1996)714:1-2<145:RRBEAT>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
SODIUM-POTASSIUM-ATPASE; EXCITATORY AMINO-ACIDS; NON-NMDA RECEPTORS; KAINIC ACID; BRAIN-DAMAGE; GLUTAMATE NEUROTOXICITY; CHRONIC INFUSION; ASPARTATE; MK-801; STRIATUM;
Keywords:
NA+/K+-ATPASE INHIBITOR; OUABAIN; EXCITOTOXIN; GLUTAMATE RECEPTOR AGONIST; GLUTAMATE RECEPTOR ANTAGONIST; NEURONAL CYTOTOXICITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
G.J. Lees e W. Leong, "RESEARCH REPORT BETWEEN EXCITOTOXINS AND THE NA+ K+-ATPASE INHIBITOR OUABAIN IN CAUSING NEURONAL LESIONS IN THE RAT HIPPOCAMPUS/", Brain research, 714(1-2), 1996, pp. 145-155

Abstract

A possible indirect role of glutamate in causing the neuronal death found after intracerebral administration of a low dose of ouabain (0.1 nmol) has been evaluated. This dose of ouabain produces a more extensive neuronal lesion than those caused by glutamate receptor agonists (kainate at an equimolar dose, or NMDA (N-methyl-D-aspartate) at a 50-fold higher dose). The selective glutamate receptor antagonists, dizocilpine (MK-801) and NBQX ihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline), in doses which blocked the direct toxicity of glutamate receptor agonists acting on either the NMDA and non-NMDA classes of glutamate receptor, failed to provide more than a minor protection against ouabain-induced neuronal death in the rat dorsal hippocampus. In contrast, the non-selective glutamate receptor antagonist, kynurenate (100 nmol) reduced the damage by around 70%. The difference in neuroprotection found between the glutamate receptor antagonists suggests that kynurenatemay protect by a non-glutamatergic mechanism. Co-administration of ouabain and glutamate receptor agonists (kainate, NMDA or glutamate) resulted in additive rather than synergistic damage to hippocampal neurons. The results suggest that in vivo, ouabain and excitotoxins probablycause neuronal death by independent mechanisms.

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Documento generato il 15/07/20 alle ore 14:17:46