The non-NMDA antagonists, NBQX and GYKI 52466, protect against cortical and striatal cell loss following transient global ischaemia in the rat.

The cerebroprotective action of non-NMDA receptor blockade has been assessed in a model of transient global ischaemia using NBQX, 2,3-dihydro-6-nitro-7-sulphamoyl-benzo(F)quinoxaline, and GYKI 52466, 1-(amino-phenyl)-4-methyl-7,8-methylendioxy-5H-2,3-benzodiazepine. HCl. In Wistar rats, prior cauterisation of the vertebral arteries was followed by occlusion of the common carotid arteries for 20 min, with a 7 day survival period before histological evaluation. NBQX, 40 mg/kg, or GYKI 52466, 40 mg/kg, was administered intravenously starting directly after the end of carotid occlusion and ending 3 h later. Both compounds produced significant protection against selective cell loss in the striatum and cortex. Less consistent changes were seen in the hippocampus; protection by NBQX was significant in CA3 but neither compound produced significant protection in CA1. This pattern of protection is interpreted in terms of a blockade of glutamate's action at non-NMDA receptors limited to the initial 3 h of reperfusion.