Temporal Patterns of Uncoupling Between Oxidative Metabolism and Regional Cerebral Blood Flow Demonstrated by Functional Magnetic Resonance Imaging

Hedera, Peter; Wu, Dee H.; Lewin, Jonathan S.; Miller, David A.; Lerner, Alan J.; Friedland, Robert P.

doi:10.1097/00004424-199511000-00001

Cited by 9 publications

(6 citation statements)

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“…In contrast, Fox et al (1988) and Fox and Raichle (1986), using PET, reported that, upon activation, brain regions increase their levels of blood flow and glucose utilization by 53-55% while oxygen consumption increases only by 5%. A similar, but less pronounced mismatch between glucose and oxygen consumption during activation was found in several subsequent studies in animals and humans (Ackerman and Lear, 1989;Fellows et al, 1993;Hedera et al, 1995;Madsen et al, 1999;Pritchard et al, 1991;Sappey-Marinier et al, 1992). A similar, but less pronounced mismatch between glucose and oxygen consumption during activation was found in several subsequent studies in animals and humans (Ackerman and Lear, 1989;Fellows et al, 1993;Hedera et al, 1995;Madsen et al, 1999;Pritchard et al, 1991;Sappey-Marinier et al, 1992).…”

Section: Coupling Of Blood Flow and Oxidative Metabolism During Physisupporting

confidence: 58%

Cellular pathways of energy metabolism in the brain: Is glucose used by neurons or astrocytes?

Nehlig

Coles

2007

Glia

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Most techniques presently available to measure cerebral activity in humans and animals, i.e. positron emission tomography (PET), autoradiography, and functional magnetic resonance imaging, do not record the activity of neurons directly. Furthermore, they do not allow the investigator to discriminate which cell type is using glucose, the predominant fuel provided to the brain by the blood. Here, we review the experimental approaches aimed at determining the percentage of glucose that is taken up by neurons and by astrocytes. This review is integrated in an overview of the current concepts on compartmentation and substrate trafficking between astrocytes and neurons. In the brain in vivo, about half of the glucose leaving the capillaries crosses the extracellular space and directly enters neurons. The other half is taken up by astrocytes. Calculations suggest that neurons consume more energy than do astrocytes, implying that astrocytes transfer an intermediate substrate to neurons. Experimental approaches in vitro on the honeybee drone retina and on the isolated vagus nerve also point to a continuous transfer of intermediate metabolites from glial cells to neurons in these tissues. Solid direct evidence of such transfer in the mammalian brain in vivo is still lacking. PET using [(18)F]fluorodeoxyglucose reflects in part glucose uptake by astrocytes but does not indicate to which step the glucose taken up is metabolized within this cell type. Finally, the sequence of metabolic changes occurring during a transient increase of electrical activity in specific regions of the brain remains to be clarified.

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Section: Coupling Of Blood Flow and Oxidative Metabolism During Physisupporting

confidence: 58%

Cellular pathways of energy metabolism in the brain: Is glucose used by neurons or astrocytes?

Nehlig

Coles

2007

Glia

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“…After that, the situation of maximal activation is likely exceeding the need of the task and a decrease is detected, probably associated with the abovementioned recoupling between CBF and CMRO 2 . This tendency to the recoupling of hemodynamic parameters after prolonged stimulation is also attested in Hedera et al 71 Moreover, one of the phenomena most frequently encountered in the study of sustained attention is habituation: Against a gradual decrease in the neurohemodynamic activation, behavioral performance of the examinee remains stable. 72,73 In other words, the brain progressively automates the carrying out of the task and gradually reduces the energetic request, without negatively affecting the performance.…”

Section: Ivb Discussion Of Resultsmentioning

confidence: 60%

Effect of prolonged stimulation on cerebral hemodynamic: A time‐resolved fNIRS study

et al. 2009

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“…Increased lactate concentration under conditions of increased brain activity (Prichard et al, 1991) is generally consistent with this idea. Numerous studies using blood oxygenation-dependent functional imaging have shown that during local activation the tissue actually experiences an increased oxygen tension (Hedera et al, 1995;Ances et al, 2001;Hyder et al, 2002;Trü bel et al, 2006). We have explained the lactate increase in the presence of plentiful oxygen by suggesting that the rapid energy requirements for ATP cannot be met by normal oxidative metabolism, which proceeds more slowly .…”

Section: Discussionmentioning

confidence: 79%

Neuronal–Glial Glucose Oxidation and Glutamatergic–GABAergic Function

Hyder

Patel

Gjedde

et al. 2006

J Cereb Blood Flow Metab

371

399

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Prior 13C magnetic resonance spectroscopy (MRS) experiments, which simultaneously measured in vivo rates of total glutamate-glutamine cycling (V(cyc(tot))) and neuronal glucose oxidation (CMR(glc(ox), N)), revealed a linear relationship between these fluxes above isoelectricity, with a slope of approximately 1. In vitro glial culture studies examining glutamate uptake indicated that glutamate, which is cotransported with Na+, stimulated glial uptake of glucose and release of lactate. These in vivo and in vitro results were consolidated into a model: recycling of one molecule of neurotransmitter between glia and neurons was associated with oxidation of one glucose molecule in neurons; however, the glucose was taken up only by glia and all the lactate (pyruvate) generated by glial glycolysis was transferred to neurons for oxidation. The model was consistent with the 1:1 relationship between DeltaCMR(glc(ox), N) and DeltaV(cyc(tot)) measured by 13C MRS. However, the model could not specify the energetics of glia and gamma-amino butyric acid (GABA) neurons because quantitative values for these pathways were not available. Here, we review recent 13C and 14C tracer studies that enable us to include these fluxes in a more comprehensive model. The revised model shows that glia produce at least 8% of total oxidative ATP and GABAergic neurons generate approximately 18% of total oxidative ATP in neurons. Neurons produce at least 88% of total oxidative ATP, and take up approximately 26% of the total glucose oxidized. Glial lactate (pyruvate) still makes the major contribution to neuronal oxidation, but approximately 30% less than predicted by the prior model. The relationship observed between DeltaCMR(glc(ox), N) and DeltaV(cyc(tot)) is determined by glial glycolytic ATP as before. Quantitative aspects of the model, which can be tested by experimentation, are discussed.

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Temporal Patterns of Uncoupling Between Oxidative Metabolism and Regional Cerebral Blood Flow Demonstrated by Functional Magnetic Resonance Imaging

Cited by 9 publications

References 0 publications

Cellular pathways of energy metabolism in the brain: Is glucose used by neurons or astrocytes?

Cellular pathways of energy metabolism in the brain: Is glucose used by neurons or astrocytes?

Effect of prolonged stimulation on cerebral hemodynamic: A time‐resolved fNIRS study

Neuronal–Glial Glucose Oxidation and Glutamatergic–GABAergic Function

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