Mild postischemic hypothermia is neuroprotective in the immature rat neocortex slice

Immature rat brain slices exposed to oxygen–glucose deprivation as an in vitro model of neonatal hypoxic–ischemic encephalopathy

“…It has been demonstrated that OGD-exposed slices is a useful in vitro model to study ischemic brain injury in adult rats (Lizasoain et al, 1996;Moro et al, 1998;De Alba et al, 1999;Cárdenas et al, 2000;Hurtado et al, 2001); the present work extends this conclusion to immature rats. Previous works exposing forebrain slices of immature rats to OGD have demonstrated that OGD affects neuronal activity, as reflected by inositol phosphate formation (Cristofol et al, 1996), mithochondrial activity (Brooks et al, 2000) or field potential changes (Ko et al, 2001); these studies, however, have not studied the involvement of excitotoxicity or cytokines release in this process. Other studies have described OGD-induced injury in immature brain, as revealed by ATP tissue concentration and protein synthesis rate decrease, demonstrating both Glu release and NO activity increase in this process (Berger et al, 1998;Garnier et al, 2002); these experiments were performed on hippocampal slices from fetal guinea pigs.…”

“…From the in vitro models, the use of brain slices instead of neuronal cultures offer the additional advantage that in brain slices the tissue morphology is relatively unchanged from the intact animal structure since intercellular connections are preserved (Lizasoain et al, 1996;Moro et al, 1998;De Alba et al, 1999;Cárdenas et al, 2000;Hurtado et al, 2001). In immature animals, the most used in vitro model of NHIE with brain slices is the oxygen-glucose deprivation (OGD), performed either on hippocampal slices (Berger et al, 1998;Garnier et al, 2002) or forebrain slices (Cristofol et al, 1996;Brooks et al, 2000;Ko et al, 2001).…”