Respiration by Cultivated Astrocytes and Neurons From the Cerebral Hemispheres

Dittmann, L.; Sensenbrenner, M.; Hertz, Leif; Mandeli, P.

doi:10.1111/j.1471-4159.1973.tb04238.x

Cited by 39 publications

(9 citation statements)

References 25 publications

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“…(For explanation of the use of the factor 6, see Materials and Methods; the calculated rate is the absolute value if no dilution of specific activity occurs on traversal of labeled carbon through the TCA cycle, hence the calculation yields a minimal value.) This value is considerably less than the previously measured rate of oxygen uptake in cultured rat astrocytes (Dittmann et al, 1973;cf. Hertz et al, 1988), reflecting the fact that substrates in addition to glucose (most notably glutamate) are oxidized by astrocytes .…”

Section: Discussioncontrasting

confidence: 62%

Effects of Ammonia and β‐Methylene‐dl‐Aspartate on the Oxidation of Glucose and Pyruvate by Neurons and Astrocytes in Primary Culture

Fitzpatrick¹,

Cooper²,

Hertz³

1988

Journal of Neurochemistry

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Both 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.

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Section: Discussioncontrasting

confidence: 62%

Effects of Ammonia and β‐Methylene‐dl‐Aspartate on the Oxidation of Glucose and Pyruvate by Neurons and Astrocytes in Primary Culture

Fitzpatrick¹,

Cooper²,

Hertz³

1988

Journal of Neurochemistry

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“…Because of the presence of astrocytes, which have higher respiratory rates, the rates of neurons probably are less than those we are reporting. The basal rates of our cultured neurons generally are less than those previously measured in bulk-separated, microdissected, and cultured neurons (Dittman et al, 1973;Kovaru et al, 1978). The differences between these results and ours may be due to differences in species, in methods of preparing cells, and in techniques of measuring cell respiration.…”

Section: Discussioncontrasting

confidence: 50%

Respiration in Primary Cultured Cerebellar Granule Neurons and Cerebral Cortical Neurons

Jameson

Olson

Nguyen

et al. 1984

Journal of Neurochemistry

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Respiration was measured polarographically in primary cultures enriched with cerebellar granule neurons or cerebral cortical neurons. The basal respiratory rate, measured on the sixth day after culturing, was 12.00 natom equiv. O/mg protein/min for the cortical neurons and 12.70 natom equiv. O/mg protein/min for the granule neurons. Maximal stimulation by 2,4-dinitrophenol produced a 20-40% increase over the basal rate for both neuronal types. Oligomycin inhibited neuronal basal respiration by 45%. These respiratory rates in neurons from primary culture are markedly lower than those measured in astrocytes grown under similar conditions.

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“…This value is comparable to the rate of glucose utilization in mouse brain [41] and only two times higher than a value of 2.2 µmol O 2 /min per mg wet wt. determined in cultured rat astrocytes dissected from slightly different cultures and measured by micromanometry [62]. Olson and Holtzman [60] observed a slightly lower value, i.e., 1.7 µmol O 2 /min per g wet wt in their rat astrocytes.…”

Section: Glutamate and Glutamine Formation And Glutamate Oxidationmentioning

confidence: 99%

Glutamine-Glutamate Cycle Flux Is Similar in Cultured Astrocytes and Brain and Both Glutamate Production and Oxidation Are Mainly Catalyzed by Aspartate Aminotransferase

Hertz

Rothman

2017

Biology

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The glutamine-glutamate cycle provides neurons with astrocyte-generated glutamate/γ-aminobutyric acid (GABA) and oxidizes glutamate in astrocytes, and it returns released transmitter glutamate/GABA to neurons after astrocytic uptake. This review deals primarily with the glutamate/GABA generation/oxidation, although it also shows similarity between metabolic rates in cultured astrocytes and intact brain. A key point is identification of the enzyme(s) converting astrocytic α-ketoglutarate to glutamate and vice versa. Most experiments in cultured astrocytes, including those by one of us, suggest that glutamate formation is catalyzed by aspartate aminotransferase (AAT) and its degradation by glutamate dehydrogenase (GDH). Strongly supported by results shown in Table 1 we now propose that both reactions are primarily catalyzed by AAT. This is possible because the formation occurs in the cytosol and the degradation in mitochondria and they are temporally separate. High glutamate/glutamine concentrations abolish the need for glutamate production from α-ketoglutarate and due to metabolic coupling between glutamate synthesis and oxidation these high concentrations render AAT-mediated glutamate oxidation impossible. This necessitates the use of GDH under these conditions, shown by insensitivity of the oxidation to the transamination inhibitor aminooxyacetic acid (AOAA). Experiments using lower glutamate/glutamine concentration show inhibition of glutamate oxidation by AOAA, consistent with the coupled transamination reactions described here.

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Respiration by Cultivated Astrocytes and Neurons From the Cerebral Hemispheres

Cited by 39 publications

References 25 publications

Effects of Ammonia and β‐Methylene‐dl‐Aspartate on the Oxidation of Glucose and Pyruvate by Neurons and Astrocytes in Primary Culture

Effects of Ammonia and β‐Methylene‐dl‐Aspartate on the Oxidation of Glucose and Pyruvate by Neurons and Astrocytes in Primary Culture

Respiration in Primary Cultured Cerebellar Granule Neurons and Cerebral Cortical Neurons

Glutamine-Glutamate Cycle Flux Is Similar in Cultured Astrocytes and Brain and Both Glutamate Production and Oxidation Are Mainly Catalyzed by Aspartate Aminotransferase

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