GYKI 52466 and ischemia-evoked neurotransmitter amino acid release from rat cerebral cortex

The effects of the benzodiazepine derivative GYKI 52466 on ischemia-evoked neurotransmitter amino acid release were evaluated in a rat four vessel occlusion model with cerebral cortical cups. Following intravenous GYKI 52466 administration (10 mg kg-1 bolus followed by 10 mg kg-1 60 min-1 infusion) glutamate, aspartate and GABA release into cerebral cortical superfusates was enhanced by ischemia to a comparable extent to that observed in control ischemic rats. These results suggest that the protective action of GYKI 52466 against cerebral cortical ischemic injury is unlikely to be due to a selective reduction in extracellular glutamate levels, but is rather, a result of the recognized ability of this compound to block non-NMDA receptors.