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• W1998264209 abstract "Cerebral energy metabolism was studied in brains of mice treated with the nicotinamide analog, 6-aminonicotinamide (6-AN), which is converted to a potent inhibitor of 6-phosphogluconate dehydrogenase in viro. Six hours after administration of 6-AN, the level of cerebral 6-phosphogluconate was increased at least 170-fold, whereas substrates for other NADP +-dependent dehydrogenases either did not change or increased only slightly. Large increases in 6-phosphogluconate were observed in the cerebral cortex, three layers of the cerebellum, and the dorsal column and anterior horn regions of the spinal cord after administration of 6-AN. Thus, glucose was metabolized via the oxidative enrymes of the pentose phosphate pathway in a wide variety of neuronal structures in vivo. Highest concentrations of 6-phosphogluconate were observed in the cerebellar molecular layer. Energy use rates and glycolysis were studied by measuring the disappearance of the major energy reserves during periods of anoxic-ischemia imposed on cerebral tissue of 6-AN-treated mice. Production of lactate and utilization of glycogen during anoxic-ischemia were reduced in brain of 6-AN-treated mice, which is in accord with the suggestion that glycolysis is inhibited in cerebral tissue of 6-AN-treated animals. Levels and ratios of pyridine nucleotides in cerebral tissue were not altered by 6-AN treatment. From changes in levels of ATP, phosphocreatine, glucose, and glycogen in brain during ischemia, the rate of energy use was calculated to be 21.7 mmol · kg wet tissue−1 · min−1, which was not significantly different from that observed in normal adult mouse brain. Therefore, despite an apparent slowing of hexose utilization in cerebral tissue 6-AN-treated mice, normal cerebral energy use was maintained during the initial period of anoxic-ischemia." @default.
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• W1998264209 date "1974-01-01" @default.
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• W1998264209 title "Cerebral energy reserves and glycolysis in neural tissue of 6-aminonicotinamide-treated mice" @default.
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• W1998264209 doi "https://doi.org/10.1002/neu.480050502" @default.
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