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Titolo:
Inhibition of evoked glutamate release by the neuroprotective 5-HT1A receptor agonist BAY x 3702 in vitro and in vivo
Autore:
Mauler, F; Fahrig, T; Horvath, E; Jork, R;
Indirizzi:
Bayer AG, PHR CNS, D-42096 Wuppertal, Germany Bayer AG Wuppertal GermanyD-42096 , PHR CNS, D-42096 Wuppertal, Germany
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1, volume: 888, anno: 2001,
pagine: 150 - 157
SICI:
0006-8993(20010105)888:1<150:IOEGRB>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOCAL CEREBRAL-ISCHEMIA; EXCITATORY AMINO-ACIDS; EXTRACELLULAR GLUTAMATE; ARTERY OCCLUSION; BRAIN-DAMAGE; INTRACEREBRAL MICRODIALYSIS; CHANNEL BLOCKER; NMDA ANTAGONIST; RAT STRIATUM; SEROTONIN;
Keywords:
BAY x 3702; glutamate release; ischemia; middle cerebral artery occlusion; microdialysis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Mauler, F Bayer AG, PHR CNS, Aprather Weg 18a, D-42096 Wuppertal, Germany Bayer AG Aprather Weg 18a Wuppertal Germany D-42096 al, Germany
Citazione:
F. Mauler et al., "Inhibition of evoked glutamate release by the neuroprotective 5-HT1A receptor agonist BAY x 3702 in vitro and in vivo", BRAIN RES, 888(1), 2001, pp. 150-157

Abstract

Brain ischemia provoked by stroke or traumatic brain injury induces a massive increase in neurotransmitter release, in particular of the excitotoxin glutamate. Glutamate triggers a cascade of events finally leading to widespread neuronal cell damage and death. The aminomethylchroman derivative BAY x 3702 is a novel neuroprotectant which shows pronounced beneficial effectsin various animal models of ischemic brain injury. As shown previously BAYx 3702 binds to 5-HT1A receptors of different species in subnanomolar range and is characterized as a full receptor agonist. In this study we investigated the influence of BAY x 3702 on potassium-evoked glutamate release in vitro and ischemia-induced glutamate release in vivo. In rat hippocampal slices BAY x 3702 inhibited evoked glutamate release in a dose-dependent manner (IC50 = 1 muM). This effect was blocked by the selective 5-HT1A receptorantagonist WAY 100635, indicating that BAY x 3702 specifically acts via 5-HT1A receptors. In vivo, release of endogenous aspartate and glutamate was measured in the cortex of rats by microdialysis before and after onset of permanent middle cerebral artery occlusion. Single dose administration of BAY x 3702 (1 mug/kg or 10 mug/kg i.v.) immediately after occlusion reduced the increase and total release of extracellular glutumate by about 50% compared to non-treated animals, whereas the extracellular aspartate levels werenot significantly affected. Inhibition of glutamate release may therefore contribute to the pronounced neuroprotective efficacy of BAY x 3702 in various animal models of ischemic brain damage. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 09:29:07