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Cited by 174Neuroscience and Neuropharmacology ResearchAdvanced MRI Techniques and ApplicationsTraumatic Brain Injury and Neurovascular Disturbances

The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.

Cerebral Oxygen/Glucose Ratio is Low during Sensory Stimulation and Rises above Normal during Recovery: Excess Glucose Consumption during Stimulation is Not Accounted for by Lactate Efflux from or Accumulation in Brain Tissue

Madsen, Peter Lund, Cruz, Nancy F., Sokoloff, Louis, Dienel, Gerald A.·1999·Journal of Cerebral Blood Flow & Metabolism
DOI 10.1097/00004647-199904000-00005
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Abstract

Functional activation stimulates CMRglc more than CMRO2 and raises lactate levels in brain. This has been interpreted as evidence that brain work is supported mainly by energy derived from anaerobic glycolysis. To determine if lactate production accounts for the "excess" glucose consumption, cerebral arteriovenous differences were measured in conscious rats before, during, and 15 minutes after sensory stimulation; the brains were rapidly frozen in situ immediately after completion of blood sampling and assayed for metabolite levels. The molar O2/glucose uptake ratio fell from 6.1+/-1.1 (mean+/-SD) before stimulation to 5.0+/-1.1 during activation (P<0.01); lactate efflux from brain to blood was detectable at rest but not during stimulation. By 15 minutes after activation, O2 and lactate arteriovenous differences normalized, whereas that for glucose fell, causing the O2/glucose ratio to rise above preactivation levels to 7.7+/-2.6 (P<0.01). Brain glucose levels remained stable through all stages of activity. Brain lactate levels nearly doubled during stimulation but normalized within 15 minutes of recovery. Brain glycogen content fell during activation and declined further during recovery. These results indicate that brain glucose metabolism is not in a steady state during and shortly after activation. Furthermore, efflux from and increased content of lactate in the brain tissue accounted for less than 54% of the "excess" glucose used during stimulation, indicating that a shift to anaerobic glycolysis does not fully explain the disproportionately greater increases in CMRglc above that of CMRO2 in functionally activated brain. These results also suggest that the apparent dissociation between glucose utilization and O2 consumption during functional activation reflects only a temporal displacement; during activation, glycolysis increases more than oxidative metabolism, leading to accumulation of products in intermediary metabolic pools that are subsequently consumed and oxidized during recovery.

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Crossref · 10.1097/00004647-199904000-00005

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41 of 41 references verified0 citation errors · 0 not checkable

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  • The overall OGI is reduced from near-stoichiometric values down to ∼5 during brain stimulation.

    “The overall OGI is reduced from the near-stoichiometric values down to ∼5 (Madsen et al., 1999).”

    From Fueling thought: Management of glycolysis and oxidative phosphorylation in neuronal metabolism (2018) · cites this paper as Madsen et al., 1999

  • If unstimulated tissue in the periphery or within the stimulated region is capable of oxidative metabolism of excess lactate, including its contribution will normalize the OGI.

    “For instance, if the unstimulated tissue in the periphery or even within the stimulated region is capable of oxidative metabolism of the excess lactate (Madsen et al., 1999; Gandhi et al., 2009), then including the contribution from this tissue will normalize the OGI.”

    From Fueling thought: Management of glycolysis and oxidative phosphorylation in neuronal metabolism (2018) · cites this paper as Madsen et al., 1999

  • The resting brain consumes glucose and metabolizes it nearly completely to CO2.

    “It is generally agreed that the “resting” brain, under normal metabolic circumstances, consumes glucose and metabolizes it nearly completely to CO2 (Clarke and Sokoloff, 1994; Madsen et al., 1999).”

    From Neuronal Stimulation Triggers Neuronal Glycolysis and Not Lactate Uptake (2017) · cites this paper as Madsen et al., 1999

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Research works printed but not linked: 3

  1. Ribeiro L, 1993, Ann Nucl Med, 7, S122
  2. Scremin OU, 1995, The Rat Nervous System., 3
  3. Sokoloff L, 1960, Handbook of Physiology: Neurophysiology, 3, 1843

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Metadata

Authors
Madsen, P. L., Cruz, N. F., Sokoloff, L., & Dienel, G. A.
Affiliations
National Institutes of Health (US)
Corresponding author
Sokoloff, Louis
ORCID
Dienel, Gerald A.
Venue
Journal of Cerebral Blood Flow & Metabolism
Publisher
SAGE Publications
Published
1999-04
Volume
19
Issue
4
Pages
393-400
ISSN
  • 0271-678X (ISSN-L)
  • 1559-7016
DOI
10.1097/00004647-199904000-00005
OpenAlex
W2049036645
Cited by
174
References
41
Citations by year
2026: 4 · 2025: 8 · 2024: 1 · 2023: 6 · 2022: 6 · 2021: 3 · 2020: 1 · 2019: 5 · 2018: 7 · 2017: 7 · 2016: 6 · 2015: 9 · 2014: 8 · 2013: 4 · 2012: 10
FWCI
2.05
Type
journal article
Language
en
Open access
closed
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations
  • Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced MRI Techniques and Applications
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords
brain glucose metabolism, cerebral oxygen consumption, lactate efflux, anaerobic glycolysis, functional brain activation, sensory stimulation, brain lactate, brain glycogen, cerebral blood flow
MeSH terms
Animals, Brain, Glucose, Glycolysis, Lactates, Male, Oxygen, Stimulation, Chemical, Rats, Sprague-Dawley, Rats

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