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pubmed-article:3138386pubmed:abstractTextBoth ammonia and beta-methylene-DL-aspartate (beta-MA), an irreversible inhibitor of aspartate aminotransferase activity and thus of the malate-aspartate shuttle, were found previously to decrease oxidative metabolism in cerebral cortex slices. In the present work, the possibility that ammonia and beta-MA affect energy metabolism by a common mechanism (i.e., via inhibition of the malate-aspartate shuttle) was investigated using primary cultures of neurons and astrocytes. Incubation of astrocytes for 30 min with 5 mM beta-MA resulted in a decreased production of 14CO2 from [U-14C]glucose, but did not affect 14CO2 production from [2-14C]pyruvate. Conversely, incubation of astrocytes with 3 mM ammonium chloride resulted in decreased 14CO2 production from [2-14C]pyruvate, but 14CO2 production from [U-14C]glucose was not significantly affected. Ammonium chloride had no significant effect on 14CO2 production from either [U-14C]glucose or [2-14]pyruvate by neurons. However, incubation of neurons with beta-MA or beta-MA plus ammonium chloride resulted in a approximately 45% decrease of 14CO2 production from both [U-14C]glucose and [2-14C]pyruvate. A 2-h incubation of astrocytes with beta-MA resulted in no change in ATP levels, but a 35% decrease in phosphocreatine. Similar treatment of neurons resulted in greater than 50% decrease in ATP, but had little effect on phosphocreatine. beta-MA also caused a decrease in glutamate and aspartate content of neurons, but not of astrocytes. The different metabolic responses of neurons and astrocytes towards beta-MA were probably not due to a differential inhibition of aspartate aminotransferase which was inhibited by approximately 45% in astrocytes and by approximately 55% in neurons.lld:pubmed
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pubmed-article:3138386pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:3138386pubmed:articleTitleEffects of ammonia and beta-methylene-DL-aspartate on the oxidation of glucose and pyruvate by neurons and astrocytes in primary culture.lld:pubmed
pubmed-article:3138386pubmed:affiliationDepartment of Neurology, Cornell University Medical College, New York, NY 10021.lld:pubmed
pubmed-article:3138386pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3138386pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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