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Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism
Open accessAbstract
SUMMARY Oligodendrocytes make myelin and support axons metabolically with lactate. However, it is unknown how glucose utilization and glycolysis are adapted to the different axonal energy demands. Spiking axons release glutamate and oligodendrocytes express NMDA receptors of unknown function. Here we show that the stimulation of oligodendroglial NMDA receptors mobilizes glucose transporter GLUT1, leading to its incorporation into the myelin compartment in vivo. When myelinated optic nerves from conditional NMDA receptor mutants are challenged with transient oxygen-glucose deprivation, they show a reduced functional recovery when returned to oxygen-glucose but are indistinguishable from wild-type when provided with oxygen-lactate. Moreover, the functional integrity of isolated optic nerves, which are electrically silent, is extended by preincubation with NMDA, mimicking axonal activity, and shortened by NMDA receptor blockers. This reveals a novel aspect of neuronal energy metabolism in which activity-dependent glutamate release enhances oligodendroglial glucose uptake and glycolytic support of fast spiking axons.
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TL;DR
Oligodendroglial NMDA receptor activation mobilizes GLUT1 to the cell surface/myelin and increases glucose import and lactate release, coupling axonal spiking to oligodendroglial glycolytic support. Conditional NR1 loss reduces myelin GLUT1, impairs recovery from oxygen-glucose deprivation unless lactate is supplied, and causes late axonal and neurological deficits.
Key findings
- In cultured oligodendrocytes, NMDA triggered GLUT1 surface redistribution within 30 min, blocked by D-AP5; biotinylation showed a 2-fold surface GLUT1 increase, FRET glucose sensor measurements rose from 0.56 ± 0.04 mM at baseline to 1.85 ± 0.24 mM after NMDA, and NMR showed a 24% ± 4% increase in U-13C-lactate release; MCT1 was unchanged.
- In Grin1flox/flox*Cnp1Cre/+ (NR1 cKO) optic nerves, myelin GLUT1 was reduced by 80%, recombination reached 62% ± 8% at P96, and myelin was transiently thinner at P18–P20 but normal at P70.
- After 60-min oxygen-glucose deprivation, NR1 mutant optic nerves recovered 50% less than controls; lactate reperfusion restored recovery equal to or better than glucose; wild-type nerves preincubated 16 hr with NMDA/Gly maintained high-frequency conduction better, while D-AP5/7CKA worsened it, and without NMDA, 25 Hz stimulation caused about 10% decline per min.
- Adult NR1 mutants showed faster high-frequency spinal CAP amplitude drop and slower recovery, a 1-year rotarod deficit, and at 19 months a severe neurological phenotype including hind limb clasping, hunchback, and ataxia with neuroinflammation and axonopathy in white matter tracts.
Methods
- Conditional NR1 knockout mice (Grin1flox/flox*Cnp1Cre/+) versus controls, plus primary mouse/rat OPC cultures and immunopanned oligodendrocytes; assays included immunocytochemistry, surface biotinylation, FRET glucose sensor imaging, 2-deoxyglucose uptake, NMR lactate release, myelin purification/immunoblot, immunogold EM, optic nerve CAP recordings with OGD and graded frequency, in vivo spinal cord CAP recordings, rotarod, and clinical scoring.
- Statistics used Mann-Whitney, two-tailed Student’s t tests, one-way or two-way ANOVA with Bonferroni post-test, or linear mixed effects models; significance was set at *p < 0.05, p < 0.01, *p < 0.001, with data as means ± SEM.
Limitations
- Stated: astrocytes may compensate some metabolic functions in oligodendroglial NMDA receptor mutants; acute ex vivo NMDA receptor blockade did not visibly reduce recovery from OGD, which the authors attribute to different timescales between development and pharmacology; some mechanistic data (insulin mobilization, microtubule dependence) are “data not shown.”
- Evident: findings rely on rodent optic nerve/spinal cord and cultured oligodendrocytes; axonal energy metabolism is inferred from conduction recovery and lactate rescue rather than direct ATP measurement; no human data are presented.
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“that was efficiently blocked by D-(−)-2-amino-5-phosphonopentanoic acid (D-AP5)”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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In the paper
“Activation of NMDA receptors caused a significantly increased FRET signal”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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In the paper
“whereas the abundance of MCT1 was the same”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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“we calculated a 24% ± 4% increase of U-13C-lactate release originating from U-13C6-labeled glucose”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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In the paper
“that was abolished by 7-CKA and D-AP5”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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In the paper
“revealing a 2-fold GLUT1 increase at the cell surface following 30 min NMDA stimulation”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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“quantified the uptake of 2-deoxyglucose (2DG) to confirm that NMDA elevates glucose import”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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“there were no signs of oligodendrocyte death”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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In the paper
“In contrast, monocarboxylate transporter MCT1 distribution was unaffected by NMDA”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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In the paper
“NR1 was lost by immunostaining, as shown for optic nerve”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Myelination In Vivo in the Absence of Oligodendroglial NMDA Receptors
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“i.e., 0.56 ± 0.04 mM at baseline and 1.85 ± 0.24 mM following NMDA receptor stimulation”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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“Remarkably, treatment with NMDA triggered GLUT1 redistribution in oligodendrocytes within 30 min, leading to apparent surface expression”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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“at P10, when many oligodendrocytes had matured and express Cnp1, about one-third of the floxed alleles were excised, and recombination reached 62% ± 8% at P96”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Myelination In Vivo in the Absence of Oligodendroglial NMDA Receptors
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“At the age of 19 months, NR1 mutants exhibited a severe neurological phenotype including hind limb clasping, hunchback, and ataxia”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > In Vivo Relevance of Oligodendroglial NMDA Receptor Function
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“While most white and gray matter regions in mutant mice, including optic nerves, appeared devoid of pathology within the first year (data not shown), such changes became detectable in white matter tracts of the medulla”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > In Vivo Relevance of Oligodendroglial NMDA Receptor Function
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“we observed myelin delamination and degenerating axons in cervical spinal cord sections”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > In Vivo Relevance of Oligodendroglial NMDA Receptor Function
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“We detected no overt differences between NR1 mutants and controls in spinal conduction properties or axon excitability”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > In Vivo Relevance of Oligodendroglial NMDA Receptor Function
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“we found no difference in the onset of EAE symptoms or in clinical severity”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Causality of NMDA Receptor Signaling and Glucose Metabolism in Axonal Support
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“we noted at ages P18–P20 that myelin was thinner, with fewer myelinated axons in the mutant optic nerves”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Myelination In Vivo in the Absence of Oligodendroglial NMDA Receptors
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In the paper
“all optic nerves maintained conductivity (defined as “CAP area” of 1.0) and, within minutes after OGD onset, displayed block of nerve conduction”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Functional Analysis of Myelinated Axons
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“This difference was only transient as adult (P70) NR1 mutant optic nerves “catch up” and exhibit a normal myelin sheath thickness”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Myelination In Vivo in the Absence of Oligodendroglial NMDA Receptors
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“in the absence of free extracellular Ca2+, the axonal recovery was almost 100% in control nerves yet remained significantly impaired in NR1 mutants”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Causality of NMDA Receptor Signaling and Glucose Metabolism in Axonal Support
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“CAP profiles revealed a transiently reduced conduction velocity, again only at the peak of myelination (age P19–P21) and mainly affecting small caliber axons”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Functional Analysis of Myelinated Axons
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“using lactate-containing ACSF for reperfusion, optic nerves from NR1 mutants recovered as well as control nerves and even better than in the presence of glucose”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Causality of NMDA Receptor Signaling and Glucose Metabolism in Axonal Support
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“In purified myelin from mutant brains, we found a strong reduction of GLUT1 (but not MCT1) compared to controls”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Myelination In Vivo in the Absence of Oligodendroglial NMDA Receptors
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“mutant mice were normally developed with functional white matter tracts, as shown for the optic nerve”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Myelination In Vivo in the Absence of Oligodendroglial NMDA Receptors
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“when triggered with NMDA, trafficking was expectedly calcium dependent and required a stable microtubule network”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > DISCUSSION
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“Most likely, membrane repolarization (triggered by NMDA receptor signaling and ion influx) consumes the additional ATP and leads to more glycolysis with lactate release.”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > NMDA Receptor Activation Triggers GLUT1 Surface Expression and Enhances Glucose Import in Cultured Oligodendrocytes
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“Thus, further loss of axonal conductivity was not caused by more severe myelin injury, but rather by less-efficient axonal recovery from the metabolic stress of OGD.”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Functional Analysis of Myelinated Axons
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In the paper
“In development, NMDA receptors are most abundant in oligodendrocyte precursors”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > DISCUSSION
What the sources say
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In the paper
“In myelin, NR1 is associated with NR2C and NR3A subunits that provide a weak Mg2+ block”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > DISCUSSION
What the sources say
- Not checked yetcites Burzomato et al., 2010 source
- Not checked yetcites Das et al., 1998
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In the paper
“suggesting that axons require oligodendroglial support mostly after myelination, which limits rapid axonal access to extracellular metabolites”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Functional Analysis of Myelinated Axons
What the sources say
- Not checked yetcites Nave, 2010 source
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In the paper
“These are best explained by the delay of CNS myelination”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > Functional Analysis of Myelinated Axons
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In the paper
“caused by ongoing neurodegeneration, which became visible at 10 months”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > RESULTS > In Vivo Relevance of Oligodendroglial NMDA Receptor Function
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In the paper
“For quantification, 10–12 randomly taken images from three controls and three NR1 mutants were assessed.”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > EXPERIMENTAL PROCEDURES > Immunoelectron Microscopy
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In the paper
“Oligodendroglial NMDA receptors are localized in specialized microdomains of myelinating processes”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > DISCUSSION
What the sources say
- Not checked yetcites Stirling and Stys, 2010
- Not checked yetcites Stys, 2011 source
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In the paper
“They have direct access to the vasculature, store glycogen, and rapidly respond to energy deprivation with glycogen breakdown”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > DISCUSSION
What the sources say
- Not checked yetcites Brown and Ransom, 2007
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
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In the paper
“For g-ratio analysis, 4–5 random overview pictures were taken at 8,000× magnification, 200 axons analyzed using ImageJ (images were blinded for experimenter).”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > EXPERIMENTAL PROCEDURES > Electron Microscopy and Morphometry
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In the paper
“OPCs utilized for biotinylation assays, 2-deoxyglucose uptake, or lactate release were further purified to 98.2% ± 0.3% by negative selection immunopanning (Barres et al., 1992).”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > EXPERIMENTAL PROCEDURES > Cell Culture Preparation
What the sources say
- Not checked yetcites Barres et al., 1992 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“For analysis of unmyelinated, myelinated, and ensheathed axons (defined as 1–3 uncompacted layers), 4–6 EM images with 12,000× magnification 400–700 axons were counted for each nerve.”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > EXPERIMENTAL PROCEDURES > Electron Microscopy and Morphometry
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In the paper
“astrocytes can also support axon function by releasing lactate in the white matter”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > DISCUSSION
What the sources say
- Not checked yetcites Brown and Ransom, 2007
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“Three individual experiments with 14–24 cells per condition were analyzed.”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > EXPERIMENTAL PROCEDURES > Immunocytochemistry
Strength:plain· not yet calibratedn = 3Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“After OGD control ACSF and O2 were restored and CAPs were recorded for up to 2–3 hr, responses were stabilized within 20 to 30 min.”
§ Oligodendroglial NMDA Receptors Regulate Glucose Import and Axonal Energy Metabolism > EXPERIMENTAL PROCEDURES > Optic Nerve Recordings
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The paper relies on this without support.
The average spike count rate is the key determinant of axonal ATP consumption.
“Since the average spike count rate is the key determinant of axonal ATP consumption”
The paper relies on this without support.
Constitutive overproduction of lactate would result in lactic acidosis detrimental for white matter function.
“The constitutive overproduction of lactate would result in lactic acidosis, detrimental for white matter function.”
The paper relies on this without support.
Oligodendrocytes need to know the spiking activity of myelinated axons to adapt their own energy metabolism.
“oligodendrocytes need to “know” the spiking activity of myelinated axons”
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In the citing paper
“The model is further supported by ex vivo electrophysiological recordings of compound action potentials in optic nerves under defined metabolic conditions and with the help of neuronally expressed ATP sensors (Saab et al., 2016;Trevisiol et al., 2017).”
From Downregulated expression of lactate dehydrogenase in adult oligodendrocytes and its implication for the transfer of glycolysis products to axons (2024) · cites this paper as Saab et al., 2016
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“that recombines floxed genes to virtually 100% in oligodendrocytes and up to 60% of OPCs (Madsen et al., 2016;Saab et al., 2016;Vajda et al., 2015).”
From Downregulated expression of lactate dehydrogenase in adult oligodendrocytes and its implication for the transfer of glycolysis products to axons (2024) · cites this paper as Saab et al., 2016
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“we turned to the analysis of the optic nerve, a well-myelinated white matter tract, in which all Cnp Cre recombined cells are of oligodendroglial origin (Saab et al., 2016).”
From Downregulated expression of lactate dehydrogenase in adult oligodendrocytes and its implication for the transfer of glycolysis products to axons (2024) · cites this paper as Saab et al., 2016
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“As oligodendrocytes support axonal energy metabolism and neuronal health4–7, we hypothesized that loss of myelin integrity could be an upstream risk factor for neuronal amyloid-β (Aβ) deposition, the central neuropathological hallmark of AD.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [7]
The cited source says what the claim attributes to it.
In the citing paper
“This opens the possibility that glycolytic oligodendrocytes, which are suggested to support electrically active axons with an excess of glycolysis products (Fünfschilling et al., 2012;Lee et al., 2012;Saab et al., 2016;Trevisiol et al., 2017) do so primarily by self-made pyruvate.”
From Downregulated expression of lactate dehydrogenase in adult oligodendrocytes and its implication for the transfer of glycolysis products to axons (2024) · cites this paper as Saab et al., 2016
In the citing paper
“Either glucose or lactate can be used as an energy source for white matter (Brown et al., 2001; Saab et al., 2016),”
From Fueling thought: Management of glycolysis and oxidative phosphorylation in neuronal metabolism (2018) · cites this paper as Saab et al., 2016
Citations
Cites
Zhang, Y., Chen, K., Sloan, S. A., Bennett, M. L., Scholze, A. R., O'Keeffe, S., Phatnani, H. P., Guarnieri, P., Caneda, C., Ruderisch, N., et al. (2014) · The Journal of Neuroscience · doi:10.1523/jneurosci.1860-14.2014 · Cited by 4,875 · cited 7×
“GLUT1 mRNA is more abundant in mature oligodendrocytes than in precursor cells (Zhang et al., 2014).”
InfluentialPreparation of separate astroglial and oligodendroglial cell cultures from rat cerebral tissue.
McCarthy, K. D., & de Vellis, J. (1980) · The Journal of Cell Biology · doi:10.1083/jcb.85.3.890 · Cited by 3,825
Cre reporter strains produced by targeted insertion of EYFP and ECFP into the ROSA26 locus
Srinivas, S., Watanabe, T., Lin, C.-S., William, C. M., Tanabe, Y., Jessell, T. M., & Costantini, F. (2001) · BMC Developmental Biology · doi:10.1186/1471-213x-1-4 · Cited by 3,121 · cited 1×
“Some of the mice also carried the R26-stop-EYFP reporter gene for Cre activity (RRID: IMSR_ JAX:006148) (Srinivas et al., 2001).”
The essential role of hippocampal CA1 NMDA receptor-dependent synaptic plasticity in spatial memory.
Tsien, J. Z., Huerta, P. T., & Tonegawa, S. (1996) · Cell · doi:10.1016/s0092-8674(00)81827-9 · Cited by 1,782 · cited 8×
“, 2003) were crossbred to floxed NR1 (gene symbol Grin1) mice (RRID: MGI_2175051) (Tsien et al., 1996).”
InfluentialOligodendroglia metabolically support axons and contribute to neurodegeneration
Lee, Y., Morrison, B. M., Li, Y., Lengacher, S., Farah, M. H., Hoffman, P. N., Liu, Y., Tsingalia, A., Jin, L., Zhang, P.-W., et al. (2012) · Nature · doi:10.1038/nature11314 · Cited by 1,664 · cited 5×
“This confirms that axons readily use lactate for ATP generation (Fünfschilling et al., 2012; Lee et al., 2012; Tekkök et al., 2005; Wyss et al., 2011).”
InfluentialGlycolytic oligodendrocytes maintain myelin and long-term axonal integrity
Fünfschilling, U., Supplie, L. M., Mahad, D., Boretius, S., Saab, A. S., Edgar, J., Brinkmann, B. G., Kassmann, C. M., Tzvetanova, I. D., Möbius, W., et al. (2012) · Nature · doi:10.1038/nature11007 · Cited by 1,523 · cited 5×
“This confirms that axons readily use lactate for ATP generation (Fünfschilling et al., 2012; Lee et al., 2012; Tekkök et al., 2005; Wyss et al., 2011).”
InfluentialSelf-citationNeuronal activity promotes oligodendrogenesis and adaptive myelination in the mammalian brain
Gibson, E. M., Purger, D., Mount, C. W., Goldstein, A. K., Lin, G. L., Wood, L. S., Inema, I., Miller, S. E., Bieri, G., Zuchero, J. B., et al. (2014) · Science · doi:10.1126/science.1252304 · Cited by 1,472 · cited 2×
“…signaling in oligodendrocyte differentiation and promoting myelinationhasbeensuggested, basedon in vitroobservations (Li et al., 2013; Lundgaard et al., 2013), which is compatible with neuronal activity stimulating OPC proliferation and myelination in vivo (Gibson et al., 2014; Liu et al., 2012).”
MYELINATION IN RAT BRAIN: METHOD OF MYELIN ISOLATION1
Norton, W. T., & Poduslo, S. E. (1973) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1973.tb07519.x · Cited by 1,413 · cited 2×
“Myelin was purified as described before (Norton and Poduslo, 1973) from mouse brain homogenate in 0.32 M sucrose.”
InfluentialCell death and control of cell survival in the oligodendrocyte lineage
Barres, B. A., Hart, I. K., Coles, H. S. R., Burne, J. F., Voyvodic, J. T., Richardson, W. D., & Raff, M. C. (1992) · Cell · doi:10.1016/0092-8674(92)90531-g · Cited by 1,345 · cited 2×
“3% by negative selection immunopanning (Barres et al., 1992).”
InfluentialDisruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination
Lappe-Siefke, C., Goebbels, S., Gravel, M., Nicksch, E., Lee, J., Braun, P. E., Griffiths, I. R., & Nave, K.-A. (2003) · Nature Genetics · doi:10.1038/ng1095 · Cited by 1,036 · cited 8×
“Oligodendroglial metabolic support can explain why myelinated axons are vitally dependent on myelin integrity, independent of the myelin function in saltatory conduction (Griffiths et al., 1998; Kassmann et al., 2007; Lappe-Siefke et al., 2003).”
InfluentialSelf-citation
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Lemcke, R., Egebjerg, C., Berendtsen, N. T., Egerod, K. L., Thomsen, A. R., Pers, T. H., Christensen, J. P., & Kornum, B. R. (2023) · eLife · doi:10.7554/elife.87515.1 · Cited by 1
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Neuro–glia communication and glycolysis
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Oligodendrogliopathy in Multiple Sclerosis
Maloui, A. B., Tamegart, L., Oukhrib, M., Ghachi, H. E., Hamdan, Y. A., Soulimani, R., & Gamrani, H. (2023) · Advances in bioinformatics and biomedical engineering book series · doi:10.4018/978-1-6684-9675-6.ch011
Oligodendroglial metabolic support of myelinated axons driven by K+ dynamics
(2024) · Nature Neuroscience · doi:10.1038/s41593-023-01559-2
Glial Cells During the Life Cycle
Walz, W. (2023) · Springer eBooks · doi:10.1007/978-3-031-48105-5_3
Role of clathrin-mediated endocytosis in myelinating oligodendrocytes
Siems, S. B. (2024) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-10475
How does Nogo-A signalling influence mitochondrial function during multiple sclerosis pathogenesis?
Nheu, D., & Petratos, S. (2024) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2024.105767 · Cited by 3
“This in turn leads to glucose transporter 1 (GLUT1) protein expression on the surface of oligodendrocytes with concomitant influx of glucose (Saab et al., 2016).”
Askar, I. C., Spenlé, C., & Bagnard, D. (2024) · Expert Opinion on Drug Discovery · doi:10.1080/17460441.2024.2382180
“Meanwhile, N-methyl-D-aspartate (NMDA) receptors have demonstrated significant and intriguing functions in promoting the supply of energetic substrates to oligodendrocytes, thereby facilitating myelin production [13].”
Ghezzi, L., Kuenen, S., Pech, U., Schoovaerts, N., Kilic, A., Poovathingal, S. K., Davie, K., Lamote, J., Praschberger, R., & Verstreken, P. (2026) · eLife · doi:10.1101/2024.12.06.627235
Ghezzi, L., Pech, U., Schoovaerts, N., Poovathingal, S. K., Davie, K., Lamote, J., Praschberger, R., & Verstreken, P. (2025) · eLife · doi:10.7554/elife.105386.1
Myelination selectively modulates BOLD signal in white matterPreprint
Gao, Y., Xu, L., Schilling, K. G., Choi, S., Chen, R., Li, Y., Li, M., Zu, Z., Ding, Z., Anderson, A. W., et al. (2025) · Research Square · doi:10.21203/rs.3.rs-6597153/v1
“In addition , the ‘lactate shuttle’ mechanism 43 may reduce oxygen demand by supplying lactate as an alternative energy source 44,45 , with NE stimulating glycogenolysis in astrocytes 46 and NMDA receptor signaling at the “axon - oligo synapse” 47 .”
Morphology of Oligodendroglial Cells
Butt, A. M., Willis, A., Stevens, R., Hunter, I., & Nishiyama, A. (2025) · Advances in neurobiology · doi:10.1007/978-3-031-87919-7_5
Ding, T., Schweickart, G., Kaiser, K., Rivaldi, A., Marchal, N., Harrington, C. A., Varghese, A., Qin, K., Kelly, B., Sunkel, B. D., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.21.677597 · Cited by 1
Jin, R., Sun, S., Liu, X., & Ge, Q. (2025) · Immunology and Cell Biology · doi:10.1111/imcb.70059
“41,42 Specific ablation of NMDA receptors in oligodendrocytes leads to metabolic decline, ultimately culminating in neurodegeneration.”
Harishankar, B., Chand, K. K., Colditz, P. B., & Wixey, J. A. (2025) · Cells · doi:10.3390/cells14221776
“Oligodendrocytes play a major role in myelination by ensheathing axons and forming functional myelin, which facilitates communication between distant brain regions [45,46].”
Vitantonio, A. T., Dimovasili, C., Liu, Y., Ye, B., Lee, J. R., Hartigan, M., Bouchard, B., Ray, M. H., Conner, B., Vaughan, K. L., et al. (2025) · Aging Cell · doi:10.1111/acel.70298
“More specifically Saab et al. (2016) showed that activation of OL glutamatergic receptors promotes glucose uptake through insertion of GLUT1 transporters into the myelin membrane in a calcium dependent manner (Krasnow and Attwell 2016; Micu et al. 2017; Saab et al. 2016).”
Philips, T., Thompson, E. G., Spead, O., Vijayakumar, B. G., Kent, E. R., Miller, S., Nwokeleme, T., Vidensky, S., Farah, M. H., & Rothstein, J. D. (2025) · Glia · doi:10.1002/glia.70113
“metabolism and culminates in the shuttling of energy metabolites to neurons via MCTs (Pellerin and Magistretti 1994; Saab et al. 2016; Philips and Rothstein 2017).”
Martinović, K., Bauer, J., Kunze, M., Berger, J., & Forss‐Petter, S. (2023) · Figshare · doi:10.6084/m9.figshare.23538886
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26675651
Tsutsui, S., Morgan, M. L., Tedford, H. W., You, H., Zamponi, G. W., & Stys, P. K. (2022) · Figshare · doi:10.6084/m9.figshare.20381763
Tsutsui, S., Morgan, M. L., Tedford, H. W., You, H., Zamponi, G. W., & Stys, P. K. (2022) · Figshare · doi:10.6084/m9.figshare.20381757
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.26726576
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.25132072
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.25919010
Kim, K.-S., Jeon, M. T., Kim, E. S., Lee, C. H., & Kim, D.-G. (2022) · Figshare · doi:10.6084/m9.figshare.21019150
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26675654
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26675648
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.26726582
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.26726585
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.26726573
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.26726570
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26675639
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.26726564
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26675645
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.25132194
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26675657
Tsutsui, S., Morgan, M. L., Tedford, H. W., You, H., Zamponi, G. W., & Stys, P. K. (2022) · Figshare · doi:10.6084/m9.figshare.20381760
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.25919073
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26675642
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.26726567
Xie, J., Lan, Y., Zou, C., He, J., Huang, Q., Zeng, J., Pan, M., Mei, Y., Luo, J., & Zou, D. (2024) · Figshare · doi:10.6084/m9.figshare.26726579
Martinović, K., Bauer, J., Kunze, M., Berger, J., & Forss‐Petter, S. (2023) · Figshare · doi:10.6084/m9.figshare.23538889
Tsutsui, S., Morgan, M. L., Tedford, H. W., You, H., Zamponi, G. W., & Stys, P. K. (2022) · Figshare · doi:10.6084/m9.figshare.20381766
Shan, F., Zhang, N., Yao, X., Li, Y., Wang, Z., Zhang, C., & Wang, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26675636
Acute, low-grade inflammation elevates white matter sensitivity to ischemiaPreprint
Mellor, A., Harper, G. M., Kelland, E. E., & Fern, R. F. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.01.07.698147
Integration of Peripheral and Central Immune Alteration in Neurodegeneration
Wali, Z., Pinky, Neha, & Parvez, S. (2026) · Springer eBooks · doi:10.1007/978-981-95-5088-3_4
Neurodegenerative Diseases and Glucose Metabolism of Neuroglial Cells
王, 书. (2026) · Advances in Clinical Medicine · doi:10.12677/acm.2026.162418
Guo, J., Cheng, Y., & Yi, M. (2026) · Scientific Reports · doi:10.1038/s41598-026-41308-6 · Cited by 1
“Mature OLs, by contrast, are metabolically active cells that support axonal energy metabolism; their dysfunction contributes to axonal degeneration independent of demyelination 15 .”
Beyond the Wiring: White Matter as a Dynamic Regulator of Brain Function and Disease
He, C., Wu, D., Du, A., & Zhang, L. (2026) · Neuroscience Bulletin · doi:10.1007/s12264-026-01605-6
“A key mechanism underlying this support is the provision of crucial metabolic sustenance to axons [29–31].”
Wellman, S. M., Guzman, K., Suematsu, N., Thai, T. T. D., Tung, T.-H., Padilla, C. G., Sridhar, S., Chen, K., Cambi, F., & Kozai, T. D. Y. (2026) · Journal of Neural Engineering · doi:10.1088/1741-2552/ae4d8b · Cited by 1
“In parallel, oligodendrocyte-mediated transfer of glycolytic lactate and glucose via MCT1 and GLUT1 transporters provides an auxiliary substrate to buffer metabolic stress [6, 69].”
Myelin Formation and Plasticity in the Central Nervous System
Pilon, J. M., & Bouslama‐Oueghlani, L. (2026) · IntechOpen eBooks · doi:10.5772/intechopen.1013216
van Hameren, G. (2018) · theses.fr (ABES) · doi:10.70675/71c15a42zb6d9z4edazb7c1zd3f51e09c949
Le cil primaire : une nouvelle cible pour la remyélinisation ?
Delfino, G. (2020) · theses.fr (ABES) · doi:10.70675/a62c179az64bfz4247zb041zc7cfc961677c
Gliogenèse hypothalamique et contrôle de la fonction de reproduction
Martin, M. J. (2021) · theses.fr (ABES) · doi:10.70675/0650653dz87dez4961z9536z23565f173f47
Microglia-nodes of Ranvier interaction during repair
Roux, T. (2020) · theses.fr (ABES) · doi:10.70675/a1319259z2b39z4d4ez9c05z261e4533646b
Life Cycle and Circadian Rhythms in Central Resident Immunity and Neuropsychiatric Pathology
Lim, Z., Nguyen, H. L., Zeng, Y., Qu, Q., Le, Y., Sun, M., Wang, X., Zhu, H., Qian, Y., Saeed, S., et al. (2026) · Neuroscience Bulletin · doi:10.1007/s12264-026-01612-7
“However, proposed mechanisms involving metabolic disturbances affecting glucose transport and lactate shuttling, while biologically plausible, require further validation in human schizophrenia contexts [81].”
Synaptic connectivity and head-direction signal integration in the mouse presubiculum
Richevaux, L. (2021) · theses.fr (ABES) · doi:10.70675/8b297dc9zb72bz4762z951dz9ab52c80ce77
Mesaoudi, A. E. (2024) · theses.fr (ABES) · doi:10.70675/f339157ez1688z4acaz87fcz0ecae062a7cc
Optical development to image brain activity at extreme depth
Suarez-Baquero, D. E. (2024) · theses.fr (ABES) · doi:10.70675/b2f8ef6ezf2b3z43edzb579z3f1b4da5b767
Pineau, L. (2023) · theses.fr (ABES) · doi:10.70675/39c790cfzdf57z416bzb9cez06eca43d9cda
Identification and characterization of Sonic Hedgehog signal for brain maintenance and repair
Russo, M. (2023) · theses.fr (ABES) · doi:10.70675/76dce8acz0153z49ecza2f8zf494f96ab226
Masson, M. L. P. (2024) · theses.fr (ABES) · doi:10.70675/7f680c8dz2453z40c7z9047z982a66a8bfd5
An improved method for high-purity isolation of oligodendrocytes from neonatal and adult mouse brain
Guo, P., Mandon, E. C., Wang, J., Mooney, M., Reddig, K. R., Vo, P., Jerome, M. C., Lotun, A., Spinelli, J. B., Gao, G., et al. (2026) · iScience · doi:10.1016/j.isci.2026.115841
Tani, A., Yagi, M., Horiuchi, N., Nagata, K., Tanaka, T., Kittaka, H., Igami, K., & Uchiumi, T. (2026) · Mitochondrion · doi:10.1016/j.mito.2026.102168
Beyond glucose: The brain may feed itself
Matute, C. (2026) · The Transmitter · doi:10.53053/xnrq3028
Self-citationMicroenvironmental Regulation of Central Nervous System Myelination and Remyelination
Wang, Y., Tan, L., Lao, L., Huang, X., Zhang, S., & Sun, H. (2026) · Journal of Integrative Neuroscience · doi:10.31083/jin43257
Mechanobiology of Myelin Generation/Regeneration in Health and Disease
Morçimen, Z. G., Missirlis, Y. F., & Sendemi̇r, A. (2026) · Results and problems in cell differentiation · doi:10.1007/978-3-032-19509-8_15
Mot, A. I., Li, Y., Dibaj, P., Tzvetanova, I. D., Gerwig, U. C., Bogale, T. A., Goebbels, S., Möbius, W., Bergles, D. E., Morrison, B. M., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.06.09.731100
Self-citationCortical and white matter myelination proceed in concert during early infancy
Zika, S., Chang, K., Orhon, A., Kruper, J., Tyagi, C., Yan, X., Tung, S. S., Kalanit Grill-spector, A., Rokem, A., & Grotheer, M. (2026) · Nature Communications · doi:10.1038/s41467-026-73366-9 · Cited by 2
“As such, the local availability of these resources, coupled with support from glial cells like astrocytes could concurrently in fl u-ence myelination in both tissues 83,84 .”
Izagirre‐Urizar, L., Mora-Huerta, L., Soler-Sáez, I., Morales‐Gallel, R., Masson, M. L. P., Ulloa-Navas, M. J., Chara, J. C., Calovi, S., Deboux, C., Merino‐Cacho, L., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-74488-w · Cited by 4
“Myelinatingoligodendrocyteshavebeenconsideredforalongtime as lactate producers rather than consumers, and as cells that predominantly rely on glucose consumption, the rate of which depends on axonal activity 47,48 .”
Self-citationMyelin Repair as a Neuroprotective Strategy for Multiple Sclerosis: From Bench to Bedside
Battah, T., Mastorodemos, V., Struecker, E., Mitsikostas, D. D., & Papadopoulos, D. (2026) · Medicina · doi:10.3390/medicina62061183
“OLs provide axons with glycolytic aerobic metabolites, notably lactate, through the myelinic monocarboxylate transporter 1 (MCT1) (Figure 4) [68–70].”
Pérez-Villavicencio, J., Villa-Robledo, O., Megchun-Vázquez, X., Uriarte-Jiménez, F., Rubio‐Osornio, M., & Serrano‐García, N. (2026) · Neuroglia · doi:10.3390/neuroglia7030023
“…metabolic loop may arise from reduced oligodendroglial lactate support, potentially involving monocarboxylate transporter 1 (MCT1)-dependent mechanisms that are thought to be important for axonal energy homeostasis [51–53], and for which reduced expression has been reported in HD models [54].”
Fraer, A., Saleh, S., Tasabehji, D., Sharma, D. S., & Mokadem, M. (2026) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2026.1857087 · Cited by 1
“Oligodendrocytes and their precursors (OPCs) support axonal integrity and energy metabolism, with important implications for white matter integrity (Nave and Werner, 2014; Saab et al., 2016).”
Olayemi, O. E., Anthony, E. C., Edema, V. B., & Oyesola, O. (2026) · Advances in Biomedical and Health Sciences · doi:10.4103/abhs.abhs_111_25
Park, J., Cheon, S. Y., & Guo, F. (2026) · Glia · doi:10.1002/glia.70211 · Cited by 1
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Yi, Y., Chen, C., He, Y., Yu-zhou, S., Cheng, R., Liu, M., Liu, Z., & Zhang, X. (2026) · Medicinal Research Reviews · doi:10.1002/med.70103
Xiaoling, L., Yi, R., Ke, Z., Zhang, Y., & Zhou, L. (2026) · CNS Neuroscience & Therapeutics · doi:10.1002/cns.71157
Zhao, S., Sui, S., Guo, X., Ji, X., Liu, T., & Yang, H. (2026) · Cells · doi:10.3390/cells15181672
“Depletion of canonical myelinating oligodendrocytes likely compromises metabolic support to long-range hypothalamic axons governing systemic glucose homeostasis and satiety, creating a localized energy crisis that exacerbates neuronal dysfunction [56,57].”
Oligodendrocytes in central nervous system health and disease
Ryan, L. J., & Miron, V. E. (2026) · Cell · doi:10.1016/j.cell.2026.08.003
Tan, R., Lu, W., Yang, A., 杜俊清, Xu, X., Zhao, X., Qiu, M., & Tian, Y. (2026) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2026.1966652
Wang, R., Yang, Q., Cao, Z., Zhou, J., Tian, B., Wang, X., Zhang, X., Xiang, Q., & Chen, G. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1859981
Metadata
- Authors
- Saab, A. S., Tzvetavona, I. D., Trevisiol, A., Baltan, S., Dibaj, P., Kusch, K., Möbius, W., Goetze, B., Jahn, H. M., Huang, W., Steffens, H., Schomburg, E. D., Pérez-Samartín, A., Pérez-Cerdá, F., Bakhtiari, D., Matute, C., Löwel, S., Griesinger, C., Hirrlinger, J., Kirchhoff, F., & Nave, K.-A.
- Affiliations
- University of Zurich (CH)
- Max Planck Institute of Experimental Medicine (DE)
- Cleveland Clinic (US)
- Nanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 (DE)
- University of Göttingen (DE)
- Max Planck Institute for Biophysical Chemistry (DE)
- University of the Basque Country (ES)
- Corresponding author
- Kirchhoff, Frank
- Nave, Klaus-Armin
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2016-07
- Volume
- 91
- Issue
- 1
- Pages
- 119-132
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC9084537
- OpenAlex
- W2419165202
- Semantic Scholar
- 35212334fda129fe29657b347be129741e5f6e4f
- Cited by
- 590
- References
- 60
- Citations by year
- 2026: 48 · 2025: 68 · 2024: 80 · 2023: 61 · 2022: 65 · 2021: 73 · 2020: 58 · 2019: 41 · 2018: 41 · 2017: 45 · 2016: 9
- FWCI
- 25.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- PubMed Central (acceptedVersion)
- GRO (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- National Institute on Aging (R56AG033720, R01AG033720)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- glucose uptake, GLUT1, axonal energy metabolism, myelin, optic nerve, oxygen-glucose deprivation, lactate, glycolysis, glutamate release, myelination
- MeSH terms
- Animals, Axons, Energy Metabolism, Glucose, Mice, Transgenic, Myelin Sheath, Oligodendroglia, Optic Nerve, Oxygen, Receptors, N-Methyl-D-Aspartate, Glucose Transporter Type 1
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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