The role of myelin and oligodendrocytes in axonal energy metabolism

Saab, Aiman S.; Tzvetanova, Iva D.; Nave, Klaus‐Armin

doi:10.1016/j.conb.2013.09.008

Cited by 285 publications

(242 citation statements)

References 62 publications

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“…However, work in the last decade has shown that both OLs and Schwann cells solve this problem by metabolically supporting neurons, for example by providing lactate to neurons for ATP generation (Saab et al, 2013;Simons and Nave, 2015) and by regulating angiogenesis during development (Yuen et al, 2014). In fact, several of the most highly expressed proteins found in myelin are dispensable for myelination but are required in OLs/Schwann cells for axonal health.…”

Section: Mechanism and Novel Roles Of Myelinationmentioning

confidence: 99%

“…The importance of OLs in the pathology of demyelinating diseases such as MS is easily appreciated, as myelin loss directly affects nerve transmission. More broadly, the dysregulation of OL-mediated metabolic support of neurons might contribute to neuronal death in multiple neurodegenerative diseases, including MS and amyotrophic lateral sclerosis (ALS; Saab et al, 2013), as well as contributing to psychiatric disorders (Fields, 2008). Similarly, many diseases of the PNS are due primarily to pathologies of Schwann cells and a subsequent loss of neurons.…”

Section: Central Roles Of Glia In Injury Regeneration and Diseasementioning

confidence: 99%

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Glia in mammalian development and disease

2015

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Glia account for more than half of the cells in the mammalian nervous system, and the past few decades have witnessed a flood of studies that detail novel functions for glia in nervous system development, plasticity and disease. Here, and in the accompanying poster, we review the origins of glia and discuss their diverse roles during development, in the adult nervous system and in the context of disease.

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Section: Mechanism and Novel Roles Of Myelinationmentioning

confidence: 99%

Section: Central Roles Of Glia In Injury Regeneration and Diseasementioning

confidence: 99%

Glia in mammalian development and disease

2015

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“…Myelinated axons survived longer than oligodendrocytes in a mouse model of primary oligodendropathy, suggesting that the myelin sheath can remain supportive for axons independently from oligodendrocytes. 14 The protective effect of cilostazol against white matter injury might be selective to myelin, but not to oligodendrocytes. However, the selective protective effect of cilostazol needs to be confirmed in other experimental design using different animal models.…”

Section: Loss Of Oligodendrocytes and Attenuated Myelin Density Inducmentioning

confidence: 99%

Characterization of White Matter Injury in a Rat Model of Chronic Cerebral Hypoperfusion

Choi

Kim

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et al. 2016

Stroke

100

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Background and Purpose-Chronic cerebral hypoperfusion can lead to ischemic white matter injury resulting in vascular dementia. To characterize white matter injury in vascular dementia, we investigated disintegration of diverse white matter components using a rat model of chronic cerebral hypoperfusion. Methods-Chronic cerebral hypoperfusion was modeled in Wistar rats by permanent occlusion of the bilateral common carotid arteries. We performed cognitive behavioral tests, including the water maze task, odor discrimination task, and novel object test; histological investigation of neuroinflammation, oligodendrocytes, myelin basic protein, and nodal or paranodal proteins at the nodes of Ranvier; and serial diffusion tensor imaging. Cilostazol was administered to protect against white matter injury. Results-Diverse cognitive impairments were induced by chronic cerebral hypoperfusion. Disintegration of white matter was characterized by neuroinflammation, loss of oligodendrocytes, attenuation of myelin density, structural derangement at the nodes of Ranvier, and disintegration of white matter tracts. Cilostazol protected against cognitive impairments and white matter disintegration. Conclusions-White matter injury induced by chronic cerebral hypoperfusion can be characterized by disintegration of diverse white matter components. Cilostazol might be a therapeutic strategy against white matter disintegration in patients with vascular dementia.

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“…It is well known that astrocytes are the major energy source for neurons because they take up glucose through Gluts and provide the metabolite lactate for neurons through the 'MCT-mediated astrocyte neuron lactate shuttle' Magistretti, 1994, 2012). Similarly, oligodendrocytes can absorb extracellular glucose and/or lactate through Glut1 (also known as SLC2A1) and MCT1, respectively (Hirrlinger and Nave, 2014;Morrison et al, 2013;Rinholm et al, 2011;Saab et al, 2013). By contrast, OPCs do not express MCT1 (Lee et al, 2012), and there is a lack of evidence showing the expression of other Gluts in OPCs.…”

Section: Introductionmentioning

confidence: 99%

Connexin-based channels contribute to metabolic pathways in the oligodendroglial lineage

Niu

et al. 2016

Journal of Cell Science

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Oligodendrocyte precursor cells (OPCs) undergo a series of energyconsuming developmental events; however, the uptake and trafficking pathways for their energy metabolites remain unknown. In the present study, we found that 2-NBDG, a fluorescent glucose analog, can be delivered between astrocytes and oligodendrocytes through connexin-based gap junction channels but cannot be transferred between astrocytes and OPCs. Instead, connexin hemichannel-mediated glucose uptake supports OPC proliferation, and ethidium bromide uptake or increase of 2-NBDG uptake rate is correlated with intracellular Ca 2+ elevation in OPCs, indicating a Ca 2+ -dependent activation of connexin hemichannels. Interestingly, deletion of connexin 43 (Cx43, also known as GJA1) in astrocytes inhibits OPC proliferation by decreasing matrix glucose levels without impacting on OPC hemichannel properties, a process that also occurs in corpus callosum from acute brain slices. Thus, dual functions of connexin-based channels contribute to glucose supply in oligodendroglial lineage, which might pave a new way for energymetabolism-directed oligodendroglial-targeted therapies.

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The role of myelin and oligodendrocytes in axonal energy metabolism

Cited by 285 publications

References 62 publications

Glia in mammalian development and disease

Glia in mammalian development and disease

Characterization of White Matter Injury in a Rat Model of Chronic Cerebral Hypoperfusion

Connexin-based channels contribute to metabolic pathways in the oligodendroglial lineage

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