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- W2776309110 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 effects in various animal models of ischemic brain injury. As shown previously BAY x 3702 binds to 5-HT receptors of different species in subnanomolar range 1A 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 (IC 51 mM). This effect was blocked by the selective 5-HT receptor antagonist WAY 100635, indicating 50 1A that BAY x 3702 specifically acts via 5-HT receptors. In vivo, release of endogenous aspartate and glutamate was measured in the 1A cortex of rats by microdialysis before and after onset of permanent middle cerebral artery occlusion. Single dose administration of BAY x 3702 (1 mg / kg or 10 mg / kg i.v.) immediately after occlusion reduced the increase and total release of extracellular glutamate by about 50% compared to non-treated animals, whereas the extracellular aspartate levels were not 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. © 2001 Elsevier Science B.V. All rights reserved." @default.
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- W2776309110 date "2001-01-01" @default.
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- W2776309110 title "Research report Inhibition of evoked glutamate release by the neuroprotective 5-HT 1A receptor agonist BAY x 3702 in vitro and in vivo" @default.
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