Neurovascular toxicity of N-methyl-d-aspartate is markedly enhanced in the developing mouse central nervous system.

Penumbral perfusion is critical to brain viability. Proximal arterial occlusion and deep brain stroke has variable effect on cortical dysfunction. Cortical microvessel collaterals may be recruited and at times sufficient for partial parenchymal perfusion. Postnatal neural and endothelial cells are markedly vulnerable to glutamate excitotoxicity. Early vascular cell stress may promote partial protective neural preconditioning though postnatally a developmental window of the cerebral microvasculature may be particularly vulnerable to injury. We tested the hypothesis that postnatal NMDA excitotoxic injury, when cerebral endothelial cells' central energy source is via glycolysis, is age specific. Neurovascular responses of cortical viability were directly identified with diffuse reflectance patterns of perfusion properties in a non-invasive manner, over time. Histological evaluation for neural and vascular cytoarchitectonic abnormalities were evaluated 4- 7days post injury. Optical diffuse reflectance recordings were obtained at the injection site prior to, immediately after and 48h post injury. Extent of neurovascular injury at the infarct zone was greatest at PND 5 and cortical perfusion responses identified with recordings of pattern change. These data further suggest excitotoxic injury to both neural and vascular cells, in vivo, can enhance CNS injury in the young and neuroprotective strategies may benefit from vascular directed therapies.