Transmission Electron Microscopy and Morphometry of the CNS White Matter

Edgar, Julia M.; Smith, Rebecca Sherrard; Duncan, Ian D.

doi:10.1007/978-1-0716-0585-1_18

Cited by 7 publications

(8 citation statements)

References 37 publications

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“…This was carried out as described previously (Edgar et al, 2020 ; Thomson et al, 2006 ). Briefly, cultures were fixed in 2% paraformaldehyde/5% glutaraldehyde in 0.08 M sodium cacodylate buffer, pH 7.2, processed, sectioned and stained for electron microscopy and imaged using a JEOL JEM‐100CX II electron microscope.…”

Section: Methodsmentioning

confidence: 99%

Río‐Hortega's drawings revisited with fluorescent protein defines a cytoplasm‐filled channel system of CNS myelin

et al. 2021

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A century ago this year, Pío del Río‐Hortega (1921) coined the term ‘oligodendroglia’ for the ‘interfascicular glia’ with very few processes, launching an extensive discovery effort on his new cell type. One hundred years later, we review his original contributions to our understanding of the system of cytoplasmic channels within myelin in the context of what we observe today using light and electron microscopy of genetically encoded fluorescent reporters and immunostaining. We use the term myelinic channel system to describe the cytoplasm‐delimited spaces associated with myelin; being the paranodal loops, inner and outer tongues, cytoplasm‐filled spaces through compact myelin and further complex motifs associated to the sheath. Using a central nervous system myelinating cell culture model that contains all major neural cell types and produces compact myelin, we find that td‐tomato fluorescent protein delineates the myelinic channel system in a manner reminiscent of the drawings of adult white matter by Río‐Hortega, despite that he questioned whether some cytoplasmic figures he observed represented artefact. Together, these data lead us to propose a slightly revised model of the ‘unrolled’ sheath. Further, we show that the myelinic channel system, while relatively stable, can undergo subtle dynamic shape changes over days. Importantly, we capture an under‐appreciated complexity of the myelinic channel system in mature myelin sheaths.

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Section: Methodsmentioning

confidence: 99%

Río‐Hortega's drawings revisited with fluorescent protein defines a cytoplasm‐filled channel system of CNS myelin

et al. 2021

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“…Next, we assessed differences in myelin or axonal health, critical parameters in myelin biogenesis, and neurodegeneration ( Edgar et al., 2020 ; Peters, 2009 ). The relative volume of abnormal myelin, which included decompacted and redundant myelin, but not normal compact myelin, was decreased in FKN-infused animals ( Figures 6 K and S5 F).…”

Section: Resultsmentioning

confidence: 99%

Fractalkine enhances oligodendrocyte regeneration and remyelination in a demyelination mouse model

et al. 2023

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“…Ultrathin 80 nm sections were cut (Leica Ultra-cut UCT7), stained with uranyl acetate and lead citrate, and imaged (Japan JEM-1011 microscope). Axon diameter, myelin thickness, and the percentage of myelinated fibers were evaluated using methodology published in literature [ 79 ]. Specifically, 8-10 random non-overlapping electron micrographs at 12000 × magnification per mouse (3 mice/group) were analyzed.…”

Section: Methodsmentioning

confidence: 99%

Seipin deficiency-induced lipid dysregulation leads to hypomyelination-associated cognitive deficits via compromising oligodendrocyte precursor cell differentiation

Cui,

Yang,

et al. 2024

Cell Death Dis

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Seipin is one key mediator of lipid metabolism that is highly expressed in adipose tissues as well as in the brain. Lack of Seipin gene, Bscl2, leads to not only severe lipid metabolic disorders but also cognitive impairments and motor disabilities. Myelin, composed mainly of lipids, facilitates nerve transmission and is important for motor coordination and learning. Whether Seipin deficiency-leaded defects in learning and motor coordination is underlined by lipid dysregulation and its consequent myelin abnormalities remains to be elucidated. In the present study, we verified the expression of Seipin in oligodendrocytes (OLs) and their precursors, oligodendrocyte precursor cells (OPCs), and demonstrated that Seipin deficiency compromised OPC differentiation, which led to decreased OL numbers, myelin protein, myelinated fiber proportion and thickness of myelin. Deficiency of Seipin resulted in impaired spatial cognition and motor coordination in mice. Mechanistically, Seipin deficiency suppressed sphingolipid metabolism-related genes in OPCs and caused morphological abnormalities in lipid droplets (LDs), which markedly impeded OPC differentiation. Importantly, rosiglitazone, one agonist of PPAR-gamma, substantially restored phenotypes resulting from Seipin deficiency, such as aberrant LDs, reduced sphingolipids, obstructed OPC differentiation, and neurobehavioral defects. Collectively, the present study elucidated how Seipin deficiency-induced lipid dysregulation leads to neurobehavioral deficits via impairing myelination, which may pave the way for developing novel intervention strategy for treating metabolism-involved neurological disorders.

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Transmission Electron Microscopy and Morphometry of the CNS White Matter

Cited by 7 publications

References 37 publications

Río‐Hortega's drawings revisited with fluorescent protein defines a cytoplasm‐filled channel system of CNS myelin

Río‐Hortega's drawings revisited with fluorescent protein defines a cytoplasm‐filled channel system of CNS myelin

Fractalkine enhances oligodendrocyte regeneration and remyelination in a demyelination mouse model

Seipin deficiency-induced lipid dysregulation leads to hypomyelination-associated cognitive deficits via compromising oligodendrocyte precursor cell differentiation

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