Neuroprotection with a new kynurenic acid analog in the four-vessel occlusion model of ischemia

摘要: Global forebrain ischemia results in damage to the pyramids CA1 hippocampal subfield, which is particularly vulnerable excitotoxic processes. Morphological and functional disintegration of this area leads a cognitive dysfunction neuropsychiatric disorders. Treatment with N-methyl-d-aspartate receptor antagonists widely accepted method stop advance processes concomitant neuronal death. From clinical aspect, competitive glycine- polyamine-site relatively low affinity moderate side-effects are taken into account. Endogenous kynurenic acid acts as an antagonist on obligatory co-agonist glycine site, has long been at focus neuroprotective trials. In present study, we estimated capability novel analog transient global ischemia, measuring rate pyramidal cell loss preservation long-term potentiation Schaffer collateral-CA1 synapses. The potential was reflected by significantly diminished preserved expression. effect robust event pretreatment, also when drug administered time reperfusion. This result beneficial since putative neuroprotectant proven be effective post-treatment much greater benefit.