Ontogeny of cerebral oxidative metabolism in the chick embryo.
The low cerebral energy requirements of most mammals at birth reflect an immaturity of the central nervous system, and it has been suggested that energy demands in fetuses are even less well developed than in newborns. Furthermore, fetal cerebral energy requirements are presumed to be met predominantly or exclusively by anaerobic glycolysis. To clarify these issues, we investigated cerebral oxidative metabolism in 9-, 14-, 16-, and 19-day-old chick embryos and in newly hatched peeps. Animals were decapitated and quick-frozen in liquid Freon 0--5 min post-mortem. Forebrain extracts were prepared and assayed for ATP, phosphocreatine, glucose, and lactate. Alterations in these metabolites post-decapitation were used to calculate cerebral metabolic rates (delta similar to P) and rates of maximal anaerobic glycolysis (delta lactate). Rates of lactate accumulation during cerebral ischemia increased progressively from embryonic day 9 through hatching. Cerebral metabolic rates were not different in 9-, 14-, and 15-day-old embryos, but increased steadily thereafter. The extent to which total cerebral energy utilization could be derived from anaerobic glycolysis (delta lactate/delta similar to P) increased from a low at day 9 (0.29) to a maximum at day 16 (0.78). The data suggest that, despite the low cerebral metabolic activity of the chick embryo, at no time during development is anaerobic glycolysis capable of entirely supporting the energy needs of the developing brain.
D000818:Animals; D001921:Brain / Q000196:embryology* / Q000378:metabolism; D002545:Brain Ischemia / Q000378:metabolism; D002642:Chick Embryo; D002645:Chickens; D005947:Glucose / Q000378:metabolism; D006019:Glycolysis; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D010084:Oxidation-Reduction; D010725:Phosphocreatine / Q000378:metabolism
D007773:Lactates; D010725:Phosphocreatine; D019344:Lactic Acid; D005947:Glucose