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- W1995798371 abstract "The neuroprotective potential of eliprodil (SL 82.0715), anN-methyl-d-aspartate (NMDA) receptor antagonist acting at the polyamine modulatory site, in brain trauma was examined in a rat model of lateral fluid-percussion brain injury. The volume of the lesion was assessed histologically by measuring, at 7-days post-injury, the area of brain damage at 10 coronal planes. Eliprodil (10 mg/kg i.p.) when given 15 min, 6 h and 24 h after fluid percussion (1.6 atm) and then b.i.d. for the following 6 days, reduced by 60% the volume of cortical damage. A similar neuroprotection was obtained when the first administration of eliprodil was delayed by up to 12 h after the brain insult. Moreover, when the treatment with this compound was started at 18 h post-injury, cortical damage was still significantly reduced by 33%. Autoradiographic studies showed that eliprodil treatment (10 mg/kg, i.p.), initiated 15 min after the trauma, also caused a marked reduction of the loss of the neuronal markerω1−2 (central benzodiazepine) binding sites of the increase in the glial/macrophage marker peripheral type benzodiazepine binding sites in the cerebral cortex. In contrast, dizocilpine (a blocker of the cationic channel coupled to the NMDA receptor) when administered 6 h and 24 h after fluid percussion and then b.i.d. for the following 6 days induced a non significant reduction of the volume of the lesion at the highest tolerated dose (0.6 mg/kg i.p.). These results demonstrate the neuroprotective activity of eliprodil in experimental brain trauma using neuropathology as an endpoint and indicate that three is a very large time window for therapeutic intervention, consistent with the delayed nature of the neuronal loss, in this condition." @default.
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- W1995798371 date "1993-08-01" @default.
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- W1995798371 title "Prevention by eliprodil (SL 82.0715) of traumatic brain damage in the rat. Existence of a large (18h) therapeutic window" @default.
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- W1995798371 doi "https://doi.org/10.1016/0006-8993(93)90267-q" @default.
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