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oligodendrocyte images: illustrations and micrographs. All credits and licenses listed. Click a picture to see it large; click it again to open its paper. The pictures by method and the papers by section are in the library.

Micrographs

Transmission electron micrograph of a myelinated axon in transverse section. The concentric myelin lamellae are visible surrounding the axon core. The myelin sheath is produced by an oligodendrocyte in the CNS.

user:Roadnottaken (Wikimedia Commons) · CC BY-SA 3.0

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Electron micrograph of an ependyma-derived oligodendrocyte. From Meletis et al., showing the ultrastructure of an oligodendrocyte that arose from ependymal cells after spinal cord injury.

Meletis K, Barnabe-Heider F, Carlen M, Evergren E, Tomilin N et al. (Wikimedia Commons) · CC BY 4.0

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TEM of transverse sections of rat spinal cord showing remyelination of spared axons by iPS-derived OPCs after contusive SCI. Thin remyelinating sheaths are visible around axons.

All AH, Gharibani P, Gupta S, Bazley FA, Pashai N, Chou BK et al. (Wikimedia Commons) · CC BY 4.0

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Confocal image of oligodendrocytes in adult mouse brain stained with the Rip antibody (green). Cell nuclei are counterstained with DAPI (blue). The branching processes characteristic of myelinating oligodendrocytes are visible.

Oleg Tsupykov (Wikimedia Commons) · CC BY-SA 4.0

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Semithin sections of lesioned cerebellar white matter showing that remyelination is dependent on NMDA receptor activation. Remyelinating axons show thin myelin sheaths characteristic of newly formed oligodendrocyte internodes.

Lundgaard I, Luzhynskaya A, Stockley JH, Wang Z, Evans KA, Sibson N et al. (Wikimedia Commons) · CC BY 4.0

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Ependymal cell-derived progeny after spinal cord injury. The image shows ependymal-derived cells immunoreactive for oligodendrocyte markers, demonstrating that ependymal cells can contribute oligodendrocytes to the injury response.

Meletis K, Barnabe-Heider F, Carlen M, Evergren E, Tomilin N et al. (Wikimedia Commons) · CC BY 4.0

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Bright field microscopy showing the stages of oligodendrocyte differentiation from human iPSCs (BC1 line). The progression from OPC to immature and then mature oligodendrocyte can be followed by the elaboration of processes and flattening of the cell body.

All AH, Gharibani P, Gupta S, Bazley FA, Pashai N, Chou BK et al. (Wikimedia Commons) · CC BY 4.0

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Immunofluorescence of oligodendrocytes differentiated from human iPSCs. O4 (green) marks the oligodendrocyte surface; MBP (red) marks myelin basic protein. The two markers co-localise in mature oligodendrocytes.

Yamashita T, Miyamoto Y, Bando Y, Ono T, Kobayashi S, Doi A et al. (Wikimedia Commons) · CC BY 4.0

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Monkey ESC-derived OPCs (CMK6SFF) co-cultured with rat DRG neurons demonstrate myelinogenic potency in vitro. MBP-positive (red) myelin segments wrap along axons.

Yamashita T, Miyamoto Y, Bando Y, Ono T, Kobayashi S, Doi A et al. (Wikimedia Commons) · CC BY 4.0

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OPCs and oligodendrocytes differentiated from human iPSCs (A3 line). Fluorescence images show the differentiation protocol outcome and marker expression.

Yamashita T, Miyamoto Y, Bando Y, Ono T, Kobayashi S, Doi A et al. (Wikimedia Commons) · CC BY 4.0

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Indirect immunofluorescence defining the early stages of oligodendrocyte differentiation from iPSCs into neural progenitors (NP) and glial progenitors (GP).

All AH, Gharibani P, Gupta S, Bazley FA, Pashai N, Chou BK et al. (Wikimedia Commons) · CC BY 4.0

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Overview of the segmentation approach for electron microscopic data. a, Preprocessed transmission electron microscopic data of human corpus callosum (CC). b, Semantic prediction of the preprocessed data by the trained DenseNet, returning a likelihood of each pixel to belong to either background (violet), axon (teal), or myelin (yellow). c, Post-processed final segmentation. Each instance of a fiber (axon and myelin sheath) is labelled with a different random color. d–f, Analogous to a–c, with transmission electron microscopic data of human superficial white matter (SWM). The dashed region in f is shown in g,h. The measurement of axon (g) and myelination (h) diameters is based on ellipses fitted to each structure. Points show the centroid of each structure, axes show half of the minor axis of the fitted ellipse for the axon (solid line) and myelin (dashed line). i, Measurements (SWM: n = 220,431, CC: n = 163,133) from g, h are used for statistical assessment of local ultrastructure. We treat the short axis (half of which is shown in yellow in g, h) of the fitted ellipse as the actual diameter of each structure. All scale bars are 2 µm.

Ruthig, von der Planitz, Morozova et al 2025, PLOS Biology · CC BY 4.0

PMID 40834043
IFN-responsive oligodendrocytes localize to aged white matter close to CD8+ T cells. a, Immunofluorescence staining and quantification of C4b, Serpina3n, B2m and STAT1 in CC1+ oligodendrocytes in the white matter of 3- and 24-month-old mice (C4b+CC1+, 3-month, n = 3, 24-month, n = 5; Serpina3n+CC1+, 3-month, n = 6, 24-month, n = 4; B2m+CC1+, 3-month, n = 4, 24-month, n = 4; STAT1+CC1+, 3-month, n = 5, 24-month, n = 5; data are mean ± s.e.m.). Scale bar, 20 µm; for B2m, 10 µm.

Kaya, Mattugini, Liu et al 2022, Nature Neuroscience · CC BY 4.0

PMID 36280798
Effects of repeated sevoflurane exposure on OPC proliferation, differentiation, and myelination in neonatal mice. (A) IF staining of PDGFRα (green) and BrdU (red) in the hippocampal CA1 region. Colocalized cells (yellow) are indicated by white arrows, and nuclei were counterstained with DAPI (blue) (scale bar = 100 μm). (B) Quantitative analysis of PDGFRα+ cells and PDGFRα+/BrdU+ double-positive cells; n = 3 mice/group. (C) IF staining of Olig2 (red) and CC1 (green) in the hippocampal CA1 region. Colocalized cells (yellow) are indicated by white arrows, and nuclei were counterstained with DAPI (blue) (scale bar = 100 μm). (D) Quantitative analysis of Olig2+ cells and Olig2+/CC1+ double-positive cells; n = 3 mice/group. (E) WB analysis of PDGFRα protein expression in hippocampal tissue. (F) Quantitative analysis of PDGFRα protein band intensity; n = 3 mice/group. (G) WB analysis of Olig2 and CNPase protein expression in hippocampal tissue.

Liu, Bai, Liu et al 2026, CNS Neuroscience & Therapeutics · CC BY 4.0

PMID 42423126
MBP immunoreactivity in the p15 and p28 cerebellum. a–d The p15 cerebellum is characterized by intensive immunoreactivity for MBP throughout the WM. The density of MBP-positive fibers also increased within the DCN (star in a) and the IGL of all lobules. In the proximal parts of the lobules, MBP-positive fibers are found almost up to the PCL (a, c). Distally, MBP-positive fibers do not yet reach the PCL (b, d). At the tips of the lobular WM, MBP-positive fibers branch radially in all directions (b). Arrowheads in c and d point out MBP-positive fibers running more or less parallel to the PCL. e, f In the p28 cerebellum, many MBP-positive fibers ascend through the IGL up to the PCL. Whereas they emanate at flat angles from the white matter in proximal parts of the lobules (e), more distally,

Groteklaes, Bönisch, Eiberger et al 2020, Cerebellum (London, England) · CC BY 4.0

PMID 32002802
Age-related changes in the intensity of MBP signals in the macaque brain. A, Schematic diagram illustrates the role of MBP in maintaining myelin sheath integrity. B, Representative images of immunohistochemistry (IHC) showing MBP signals (brown) in Brodmann areas BA46 and BA9, as well as layer 1 of the prefrontal cortex (PFC) in macaques at ages 5, 10, 15, and 30 years. Scale bar as indicated. C, Relative intensities of IHC MBP signals shown in panel B were quantified using ImageJ. Data are presented as mean ± SD (n = 5 macaques per age group; * p = 0.0038, unpaired t test).

Zhang, Yao, Lv et al 2026, eNeuro · CC BY 4.0

PMID 41927490
Prophylactic OM-MOG prevents the development of spinal cord neuropathology during MOG-EAE in DR2b.Ab° mice. Neuropathological analysis of spinal cord sections from prophylactic vehicle- (upper and middle panels) and OM-MOG-injected (lower panels) DR2b.Ab° mice on day 36 post-immunization for EAE. Inflammatory cell infiltration was visualized by H&E (A, D); demyelination by Luxol fast blue [(B) and enlarged inset, (E)]; axon damage by Bielschowsky's silver staining [(C) and enlarged inset, (F)]. Vehicle-treated mice show large confluent inflammatory, demyelinating lesions with axon damage typical of MOG-EAE (arrowheads). OM-MOG-vaccinated mice showed no spinal cord pathology. Scale bars 500 μM (A–F), 100 μM enlarged inserts in middle panels.

Dagkonaki, Avloniti, Evangelidou et al 2020, Frontiers in Immunology · CC BY

PMID 33329540
TDAG8 deficiency does not affect normal myelination in the mouse brain. A. The mRNA analysis of pdgfrα, cnpase and mbp expression in whole brain homogenates did not reveal differences between the TDAG8 KO and WT mice. B. Representative images of immunohistochemically stained WT and TDAG8 KO mice brains (cerebellum) show no differences in myelination between the two genotypes.

Caratis, Opiełka, Hausmann et al 2024, PLOS ONE · CC BY 4.0

PMID 38527054
Defective myelination in the ATRX-null mouse forebrain. d Immunofluorescence microscopy of P20 brain cryosections stained with anti-MOG (green) and anti-MBP (red) antibodies confirms decreased levels of these myelin proteins in the cortex (Ctx) and corpus callosum (CC) of the forebrain of AtrxFoxG1Cre mice compared to controls (Ctrl) (n = 3 animals for each genotype).

Rowland, Jiang, Shafiq et al 2023, Nature Communications · CC BY 4.0

PMID 37925436
miR-145-5p is upregulated in chronic lesion tissue from SPMS brains. a, b Luxol fast blue/hematoxylin and eosin stained human brain tissue from healthy control white matter (HCWM), and normal appearing white matter (NAWM), active and chronic inactive lesion tissue from SPMS brain. a Scale bar = 1 mm. b Magnified from (a); scale bar = 50 µm.

Kornfeld, Cummings, Yaworski et al 2024, Communications Biology · CC BY 4.0

PMID 38965401
CNP-1 immunoreactivity in the early postnatal mouse cerebellum (p0–p6). a CNP-1-positive cells in the p4 cerebellar anlage are roundish and may be found in the velum medullare (arrowheads in a) and the anteriormost parts of the cerebellar anlage. Sagittal section close to the midline; anterior is to the left. b In the brainstem, CNP-1-positive structures have a fibrous morphology at this age. c, d CNP-1-positive cells at p6. Immunoreactive cells can again be detected in the velum medullare (arrowhead in c). They can now also be seen in the nascent central WM and the nascent WM extending into t

Groteklaes, Bönisch, Eiberger et al 2020, Cerebellum (London, England) · CC BY 4.0

PMID 32002802
Astrocytic Nrf2 and cholesterol pathways are altered in chronic human brain lesions with poor remyelination potential and oligodendrocyte death. a Nrf2+ (yellow) astrocytes (GFAP+; cyan) (arrows) with Hoechst in blue. Scale bar, 100 μm. e Active caspase-3+ (yellow) oligodendrocytes (TPPP/p25+; cyan, and Olig2+; magenta) (arrows) in control (CT), remyelinated (RM), active (A) and inactive lesions (I) from multiple sclerosis (MS) cases.

Molina-Gonzalez, Holloway, Jiwaji et al 2023, Nature Communications · CC BY 4.0

PMID 37291151
Neural precursors form compact myelin sheaths after transplantation into adult or neonatal Plp1-tg mice. ( A ) Light microscopy image of beta galactosidase-positive cells in the corpus callosum (delineated) of a Plp1-tg transplant recipient, 14 days post transplantation. ( B ) Corpus callosum of another transplant recipient showing that transplanted GFP-positive neurospheres form MBP-positive myelin. ( C and D ) Electron micrographs showing that the transplanted cells generate oligodendrocytes that wrap axons with normal-appearing myelin sheaths in which the inner tongue (black arrow), periaxonal space (arrowhead)

Gruenenfelder, McLaughlin, Griffiths et al 2020, Brain · CC BY 4.0

PMID 32419025
Anti-Olig2 staining of the white matter of a healthy older individual: Both strongly (arrows) and weakly Olig2-positive nuclei are identified.

Stork L, Stephan J, Kutllovci A et al. Impaired remyelination in late-onset multiple sclerosis. Acta Neuropathol. 2025. PMID 40167776 · CC BY 4.0

PMID 40167776
ol-ipsc-if-1.tif
Fig 4. Indirect immunofluorescence marker characterization of oligodendrocyte progenitors derived from human iPS cells. Nuclei were stained with DAPI (blue). Results show reduced expression of early markers (A) A2B5 and (B) NG2 and increased protein expression of mid to late oligodendrocyte progenitors

All AH, Gharibani P, Gupta S, Bazley FA, Pashai N, Chou B-K, et al. · CC BY 4.0

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opc-nestin-a2b5-if.tif

All AH, Gharibani P, Gupta S, Bazley FA, Pashai N, Chou B-K, et al. · CC BY 4.0

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Histopathology of different demyelinating lesion activities. Panels a-c illustrate an early active demyelinating lesion, representing the initial stage of demyelination. At this stage, degradation products from both major (e.g., MBP) and minor (e.g., MAG) myelin proteins are present within phagocytes. a LFB/PAS staining reveals a demyelinated lesion containing multiple foamy macrophages. The inset shows an enlarged microscopic image of foamy macrophages with LFB-positive myelin debris; b Anti-myelin basic protein (MBP) staining of the early active lesion reflects myelin destruction and highlights numerous macrophages filled with myelin degradation products; c Anti-myelin-associated glycoprotein (MAG) staining also shows multiple macrophages containing MAG-positive degradation products, a minor myelin protein. Panels d-f depict a late active demyelinating lesion, representing the subsequent stage of demyelination, where only degradation products from major myelin proteins (e.g., MBP) can be identified within phagocytes. d LFB/PAS staining shows a completely demyelinated lesion with reactive astrogliosis and foamy macrophages; e Anti-MBP staining reflects an advanced stage of demyelination, with only a few macrophages containing MBP-positive degradation products (see inset for MBP-positive macrophages); f In contrast, no degradation products from minor myelin proteins, such as MAG, are detected within macrophages, as demonstrated by anti-MAG staining. Panels g-i present an inactive demyelinated lesion, where no active demyelination processes are observed. g LFB/PAS staining reveals a demyelinated lesion accompanied by reactive astrogliosis and foamy macrophages; h Anti-MBP staining shows newly formed, thin myelinated fibers, indicating early remyelination. However, no myelin degradation products are observed within macrophages; i Anti-MAG staining also identifies early remyelination. LFB/PAS Luxol fast blue/periodic acid-Schiff, MBP myelin basic protein, MAG myelin-associated glycoprotein, Scale bars: a, d and g 200 um; b, f and i 50 um; e and h 100 um; c 20 um

Stork, Stephan, Kutllovci et al 2025, Acta Neuropathologica · CC BY 4.0

PMID 40167776
Confocal fluorescence image of rat oligodendrocyte precursor cells (OPCs). NG-2-positive OPCs in green, GFAP-positive astrocytes in red, nuclei counterstained with Hoechst 33342 in blue. Two distinct cell types from a mixed glial culture.

Oleg Tsupykov (Wikimedia Commons) · CC BY-SA 4.0

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Confocal image of oligodendrocytes in rat brain stained for MBP (myelin basic protein, red) and DNA/nuclei (DAPI, blue). Two oligodendrocyte cell bodies are visible; myelinated axons appear as hollow 'tramlines' because MBP is absent from the axon core.

GerryShaw / EnCor Biotechnology (Wikimedia Commons) · CC BY-SA 4.0

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Myelin characterization in the cerebellum of WT and ASMko mice. (A) Electron micrographs of white matter from cerebellar lobules of WT and ASMko mice at P10, P20, and P90. Red asterisks indicate intracellular accumulation of electron-dense lipid droplets in ASMko samples; by P90, signs of fiber degeneration and axonal loss become evident (yellow arrowheads). Only transverse sections of myelinated fibers with intact axonal morphology and normally compacted myelin were included for g-ratio measurements. Scale bar: 10 um. (B) Graphs show mean +/- SEM g-ratio of myelin thickness of wt and ASMko mice at P10, P20, and P90; P10: Statistical analysis was performed using two-tailed t test. n = 4 wt, 3 ASMko, P = 0.857; P20: n = 3 per genotype, P = 0.459; P90: n = 5 per genotype, P = 0.853. (C) Scatter plot showing the relationship between g-ratio and axon diameter (< 3 um) in wt and ASMko mice. Linear regression analyses reveal no significant differences between genotypes. More than 150 fibers were analyzed from at least three mice per genotype.

Guerrero-Valero, Melgarejo, Marchena et al 2026, EMBO Molecular Medicine · CC BY 4.0

PMID 42587127 · fig. Figure EV1
Impaired differentiation of ASMko OL. ( A ) Schematic representation of the OL lineage, illustrating the progressive morphological transition from bipolar OPCs through pre-myelination OLs to highly branched, mature, and myelinating OLs, together with the stage-specific markers used in this study (Olig2, NG2, PDGFRalpha, A2B5, CNPase, O1, MBP). These markers identify successive maturation states, with Olig2 labeling the entire lineage. ( B - D ) Representative immunofluorescence images of Olig2 ( B ), NG2 ( C ), and CNPase ( D ) in the apical region of cerebellar lobules from WT and ASMko mice at P90. Scale bar: 50 um. ( E ) Representative immunofluorescence images of MBP in the retina of WT and ASMko mice after transplantation of WT or ASMko OLs onto RGCs. Scale bar: 50 um. ( G ) Representative immunofluorescence images of NG2 in 4-day differentiated OL cultures from WT or ASMko OLs treated with vehicle, and in WT OLs treated with SM. Scale bar: 50 um. ( H ) Representative immunofluorescence images of MBP in 4-day differentiated OL cultures from WT or ASMko OLs treated with vehicle, or in WT OLs treated with SM. Scale bar: 50 um.

Guerrero-Valero, Melgarejo, Marchena et al 2026, EMBO Molecular Medicine · CC BY 4.0

PMID 42587127 · fig. Figure 2
Emodin promotes OL lineage progression in the CC and hippocampal DG in VD rats. (A, B) Representative images of double-staining for NG2 and Ki67 in the CC and DG. DAPI (nuclei, blue), NG2 (OPCs, red), Ki67+ (proliferating cells, green). White arrows indicate NG2+Ki67+ proliferating OPCs. High-magnification images were taken from the CC and DG separately. Scale bar: 20 um. (C, D) The ratio of the number of NG2+Ki67+ cells to that of NG2+ cells (%) in the CC and the DG. (E, F) The ratio of the number of Olig2+CC1+ cells to that of Olig2+ cells (%) and average number of CC1+ cells per mm2 in the CC and DG regions. (G, H) Representative images of double-staining for Olig2 and CC1 in the CC and DG of the hippocampus. DAPI (nuclei, blue), Olig2 (oligodendrocyte lineage cells, green), CC1 (mature OLs, red). White arrows indicate Olig2+CC1+ mature OLs. (**p < 0.01, ***p < 0.001 vs. Control; ##p < 0.01, ###p < 0.001 vs. VD. Data are represented as mean +/- SEM, n = 5-6 rats per group, 3 brain slices per animal; CC, corpus callosum; DG, dentate gyrus).

Wang, Dong, He et al 2026, CNS Neuroscience and Therapeutics · CC BY 4.0

PMID 42745680 · fig. FIGURE 3
GDF11 promotes OPC differentiation and maturation in vitro. (A) Representative bright-field image of purified OPCs from mouse pup brains and immunofluorescence staining of Olig2 (red) with DAPI (blue) for purity assessment. Scale bar, 100 um. (B) OPCs were treated with vehicle (Veh) or GDF11 for 48 h, and cell viability was assessed by MTT assay. Data are presented as mean +/- SEM from three independent experiments (each with six technical replicates per group). (C) Real-time PCR analysis of Mbp and Cnp mRNA levels in OPC cultures after GDF11 or Veh treatment ( n = 3 independent experiments). (D) Representative immunofluorescence images of OPC differentiation after treatment with GDF11 (100 ng/mL) or Veh. Scale bar, 100 um. (E) Quantification of the relative proportion of maturing OLs after GDF11 (100 ng/mL) or Veh treatment ( n = 3 independent experiments). (F) Representative immunofluorescence images of MBP (red) showing membrane sheet area (outlined by dashed boxes) and quantification of MBP + membrane sheet area after GDF11 (100 ng/mL) or Veh treatment ( n = 3 independent experiments). The data are presented as mean +/- SEM. ** p < 0.01, *** p < 0.001; ns, not significant.

Zhang, Yan, Huang et al 2026, CNS Neuroscience & Therapeutics · CC BY 4.0

PMID 42329180 · fig. Figure 1
In vitro and in vivo differentiation of iNPC-derived OPCs into mature and myelinating oligodendrocytes. (A) Representative FACS plots for CD140a and O4 at day 48. Their expression was analyzed by flow cytometry. (B) Morphological change from OPC to mature oligodendrocyte. The dotted box indicates the area enlarged below, showing multiple elongated and highly branched processes. Scale bars: 200 um. (C) Immunofluorescence analysis of MBP+ cells in CD140a+, CD140a+/O4+ and O4+ cells at day 5 of maturation. DAPI was used as a nuclear counterstain. Scale bar: 50 um. (D) Quantification of MBP+ cells in CD140a+, CD140a+/O4+ and O4+ cells (n = 4). * p < 0.05; ns, not significant (one-way ANOVA). (E) Immunofluorescence analysis of MBP+ and PLP1+ cells ensheathing nanofibers merged with bright field and DAPI. Scale bars: 20 um. (F) Quantification of ensheathed MBP+/PLP1+ cells on nanofibers (n = 6). DAPI was used as a nuclear counterstain.

Park, Kang, Kim et al 2026, Cells · CC BY 4.0

PMID 42346094 · fig. Figure 5
Myelin sheath onset and ultrastructure is not impacted by Piezo1 loss. A) Electron microscopy images of ventral cervical spinal cord of control (fl/fl) and Piezo1 cKO mice. Scale = 1 um. B) The percent of myelinated axons is unchanged at P5 (p = 0.40), P15 (p = 0.38), and P30 (p = 0.48). n = 3-4 mice, >300 axons/mouse. C) Average myelin sheath thickness at P15 and P30, p = 0.47 at P15, p = 0.28 at P30. n = 3 mice, 189-247 sheaths/mouse. All p values comparing littermate control (Piezo1 fl/fl) and Piezo1 cKO mice using an unpaired t test with Welch correction. D) Myelin sheath thickness on small diameter axons (<2 um) at P15, p = 0.23, and P30, p = 0.49. n = 3 mice, 150-212 axons/mouse. E) Myelin sheath thickness on the large diameter axons (>2 um) at P15, p = 0.49, and P30, p = 0.47. n = 3 mice, 25-46 axons/mouse. F) Representative images of myelin outfoldings from P15 mice. Yellow arrowheads indicate myelin outfoldings. Scale bar = 1 um. G) Percent of myelin sheaths that contain outfoldings at P15, p = 0.40 and P30, p = 0.84. n = 3 mice, with 385-561 sheaths/mouse. Graph bars indicate mean and standard deviation.

Young, Galfano, Reyngoudt et al 2026, PLOS Biology · CC BY 4.0

PMID 42766666 · fig. Fig 4
Myelin sheath onset and ultrastructure is not impacted by Piezo1 loss. A) Electron microscopy images of ventral cervical spinal cord of control (fl/fl) and Piezo1 cKO mice. Scale = 1 um. B) The percent of myelinated axons is unchanged at P5 (p = 0.40), P15 (p = 0.38), and P30 (p = 0.48). n = 3-4 mice, >300 axons/mouse. C) Average myelin sheath thickness at P15 and P30, p = 0.47 at P15, p = 0.28 at P30. n = 3 mice, 189-247 sheaths/mouse. All p values comparing littermate control (Piezo1 fl/fl) and Piezo1 cKO mice using an unpaired t test with Welch's correction. D) Myelin sheath thickness on small diameter axons (<2 um) at P15, p = 0.23, and P30, p = 0.49. n = 3 mice, 150-212 axons/mouse. E) Myelin sheath thickness on the large diameter axons (>2 um) at P15, p = 0.49, and P30, p = 0.47. n = 3 mice, 25-46 axons/mouse. F) Representative images of myelin outfoldings from P15 mice. Yellow arrowheads indicate myelin outfoldings. Scale bar = 1 um. G) Percent of myelin sheaths that contain outfoldings at P15, p = 0.40 and P30, p = 0.84. n = 3 mice, with 385-561 sheaths/mouse. Graph bars indicate mean and standard deviation.

Young, Galfano, Reyngoudt et al 2026, PLOS Biology · CC BY 4.0

PMID 42766666 · fig. Fig 4
Myelin sheath onset and ultrastructure is not impacted by Piezo1 loss. A) Electron microscopy images of ventral cervical spinal cord of control (fl/fl) and Piezo1 cKO mice. Scale = 1 um. B) The percent of myelinated axons is unchanged at P5 (p = 0.40), P15 (p = 0.38), and P30 (p = 0.48). n = 3-4 mice, >300 axons/mouse. C) Average myelin sheath thickness at P15 and P30, p = 0.47 at P15, p = 0.28 at P30. n = 3 mice, 189-247 sheaths/mouse. D) Myelin sheath thickness on small diameter axons (<2 um) at P15, p = 0.23, and P30, p = 0.49. n = 3 mice, 150-212 axons/mouse. E) Myelin sheath thickness on the large diameter axons (>2 um) at P15, p = 0.49, and P30, p = 0.47. n = 3 mice, 25-46 axons/mouse. F) Representative images of myelin outfoldings from P15 mice. Yellow arrowheads indicate myelin outfoldings. Scale bar = 1 um. G) Percent of myelin sheaths that contain outfoldings at P15, p = 0.40 and P30, p = 0.84. n = 3 mice, with 385-561 sheaths/mouse.

Young, Galfano, Reyngoudt et al 2026, PLOS Biology · CC BY 4.0

PMID 42766666 · fig. Fig 4
Pbx3 Deletion Delays Myelin Gene Expression. (a) Representative immunofluorescence images of MBP staining in Ctrl and Pbx3 cKO mice at indicated ages. Scale bar: 100 um. (b) Quantification of MBP immunofluorescence intensity in cc and CTX of Ctrl and Pbx3 cKO mice at P14, P27, and P50. Statistical analyses are limited to pairwise comparisons between control and cKO mice within each matched age; no statistical tests or direct quantitative comparisons are performed across different developmental ages. Data are presented as mean +/- SEM. n = 3 mice per group. * p < 0.05, ** p < 0.01; **** p < 0.0001, Unpaired Student t-test.

Yang, Ling, Zhang et al 2026, Journal of Developmental Biology · CC BY 4.0

PMID 42783550 · fig. Figure 3
Myelin sheath onset and ultrastructure is not impacted by Piezo1 loss. A) Electron microscopy images of ventral cervical spinal cord of control (fl/fl) and Piezo1 cKO mice. Scale = 1 um. B) The percent of myelinated axons is unchanged at P5 (p = 0.40), P15 (p = 0.38), and P30 (p = 0.48). n = 3-4 mice, >300 axons/mouse. C) Average myelin sheath thickness at P15 and P30, p = 0.47 at P15, p = 0.28 at P30. n = 3 mice, 189-247 sheaths/mouse. All p values comparing littermate control (Piezo1 fl/fl) and Piezo1 cKO mice using an unpaired t test with Welch's correction. D) Myelin sheath thickness on small diameter axons (<2 um) at P15, p = 0.23, and P30, p = 0.49. n = 3 mice, 150-212 axons/mouse. E) Myelin sheath thickness on the large diameter axons (>2 um) at P15, p = 0.49, and P30, p = 0.47. n = 3 mice, 25-46 axons/mouse. F) Representative images of myelin outfoldings from P15 mice. Yellow arrowheads indicate myelin outfoldings. Scale bar = 1 um. G) Percent of myelin sheaths that contain outfoldings at P15, p = 0.40 and P30, p = 0.84. n = 3 mice, with 385-561 sheaths/mouse. Graph bars indicate mean and standard deviation.

Young, Galfano, Reyngoudt et al 2026, PLOS Biology · CC BY 4.0

PMID 42766666 · fig. Fig 4
Myelin sheath onset and ultrastructure is not impacted by Piezo1 loss. A) Electron microscopy images of ventral cervical spinal cord of control (fl/fl) and Piezo1 cKO mice. Scale = 1 um. B) The percent of myelinated axons is unchanged at P5 (p = 0.40), P15 (p = 0.38), and P30 (p = 0.48). n = 3-4 mice, >300 axons/mouse. C) Average myelin sheath thickness at P15 and P30, p = 0.47 at P15, p = 0.28 at P30. n = 3 mice, 189-247 sheaths/mouse. D) Myelin sheath thickness on small diameter axons (<2 um) at P15, p = 0.23, and P30, p = 0.49. n = 3 mice, 150-212 axons/mouse. E) Myelin sheath thickness on the large diameter axons (>2 um) at P15, p = 0.49, and P30, p = 0.47. n = 3 mice, 25-46 axons/mouse. F) Representative images of myelin outfoldings from P15 mice. Yellow arrowheads indicate myelin outfoldings. Scale bar = 1 um. G) Percent of myelin sheaths that contain outfoldings at P15, p = 0.40 and P30, p = 0.84. n = 3 mice, with 385-561 sheaths/mouse.

Young, Galfano, Reyngoudt et al 2026, PLOS Biology · CC BY 4.0

PMID 42766666 · fig. Fig 4
OPC differentiation and maturation are impaired in Rxrg-/- cultures through a Shh-dependent mechanism. (A, B) Graphs show the percentage of OPCs (A, NG2-positive cells) and mature oligodendrocytes (B, MBP-positive cells) in WT and Rxrg-/- cultures at 6 DIVs after exposure to T3 or vehicle. (C) Representative pictures of OPCs (NG2-positive cells) and mature oligodendrocytes (MBP-positive cells) in WT and Rxrg-/- cultures. (D) Percentage of MBP-positive cells in WT and Rxrg-/- cultures treated with cyclopamine or vehicle, alone or in combination with T3. Scale bar 100 um. (E, F) Expression of Mbp at mRNA (E) and protein (F) level in WT cultures treated with cyclopamine or SAG compared to untreated cells.

Baldassarro, Brassart, Fraulob et al 2026, Glia · CC BY 4.0

PMID 41934103 · fig. FIGURE 3
The majority of myelin whorls are located within oligodendrocyte cytosol and are associated with myelinated axons, as revealed by SBEM. ( A ) Workflow for SBEM imaging and analysis of P14 optic nerves, including tissue preparation, SBEM imaging (Z-step size: 35 nm), manual segmentation, and 3D reconstruction. Created in BioRender. ( B-C'') SBEM reconstruction of P14 Tfeb F/F (B-B'') and Olig2-Cre; Tfeb F/F optic nerves (C-C''). ( D and D' ) Representative SBEM sections along the z-axis of a detached whorl (D), and its reconstruction (D') in the Olig2-Cre; Tfeb F/F optic nerve. ( E and E' ) Representative SBEM sections along the z-axis of a whorl associated with a myelinated axon (E), and its reconstruction (E') in the Olig2-Cre; Tfeb F/F optic nerve. The myelin whorl is outlined in blue, while the myelinated axon is outlined in magenta. The dashed line outlines the myelin sheaths that surround the axon and myelin whorl. ( F ) Quantification of the proportion of total whorl volume to the total optic nerve volume imaged by SBEM in P14 Tfeb F/F (Cntl) and Olig2-Cre; Tfeb F/F (cKO) optic nerves. ( G ) Quantification of individual whorl size in P14 control and Tfeb cKO optic nerves. ( H ) Quantification of 'detached' (13.68% in control, 22.92% in Tfeb cKO) and 'attached' whorl percentage (86.32% in control, 77.08% in Tfeb cKO). ( I ) Schematics showing detached myelin whorls and myelin whorls associated with myelinated axons. (Scale bar, 10 um for B', B'', C' and C''; and 1 um in D, D', E, and E').

Barbosa, Bhambri, Vasquez et al 2026, Proceedings of the National Academy of Sciences of the United States of America · CC BY 4.0

PMID 42268879 · fig. Fig. 2
The majority of myelin whorls are located within oligodendrocyte cytosol and are associated with myelinated axons, as revealed by SBEM. (A) Workflow for SBEM imaging and analysis of P14 optic nerves, including tissue preparation, SBEM imaging (Z-step size: 35 nm), manual segmentation, and 3D reconstruction. (B-C'') SBEM reconstruction of P14 TfebF/F (B-B'') and Olig2-Cre; TfebF/F optic nerves (C-C''). (B) and (C) show the SBEM volume sizes and whorl densities from TfebF/F and Olig2-Cre; TfebF/F optic nerves, respectively. The reconstructed myelin whorls can be visualized by maximum projections from the top view (B' and C') and side view (B'' and C'') in TfebF/F (B' and B'') and Olig2-Cre; TfebF/F optic nerves (C' and C''). (D and D') Representative SBEM sections along the z-axis of a detached whorl (D), and its reconstruction (D') in the Olig2-Cre; TfebF/F optic nerve. (E and E') Representative SBEM sections along the z-axis of a whorl associated with a myelinated axon (E), and its reconstruction (E') in the Olig2-Cre; TfebF/F optic nerve. The myelin whorl is outlined in blue, while the myelinated axon is outlined in yellow. Scale bar, 5 um (D and E).

Barbosa, Bhambri, Vasquez et al 2026, Proceedings of the National Academy of Sciences of the United States of America · CC BY 4.0

PMID 42268879 · fig. Fig. 2.
Luxol fast blue and PLP staining of human MS white matter showing myelin blisters at the edge of a micro-diffusely abnormal white matter lesion, reflecting focal myelin disruption without overt demyelination.

Luchicchi A 2024, Annals of clinical and translational neurology · CC BY 4.0

PMID 38425098
Luxol fast blue (LFB) and proteolipid protein (PLP) immunostaining of human white matter from an MS brain, showing micro-diffusely abnormal white matter (mDAWM) with focal myelin swellings characteristic of an early pre-demyelinating lesion.

Luchicchi A 2024, Annals of clinical and translational neurology · CC BY 4.0

PMID 38425098
Immunohistochemistry for myelin basic protein (MBP) in human MS white matter showing variation in myelin density across lesion and perilesional zones, used to assess the degree of remyelination following treatment with sphingosine-1-phosphate receptor modulators.

Ricigliano VAG 2026, Frontiers in immunology · CC BY 4.0

PMID 42780639

Illustrations

NIH BioArt illustration of an oligodendrocyte showing its branching processes, which wrap around multiple axons to form the myelin sheath. Public domain image courtesy of NIAID.

Courtesy of NIAID / Ryan Kissinger (Wikimedia Commons) · Public domain

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Scientific illustration showing the four types of glial cells in the CNS: ependymal cells, astrocytes, microglia, and oligodendrocytes. The oligodendrocyte is shown with processes wrapping around axons.

Artwork by Holly Fischer (Wikimedia Commons) · CC BY 3.0

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No detectable gross abnormality in oligodendrocyte development in Zdhhc9 KO mice. ( A ) Fluorescent (upper) an

Jeong, Gonzalez-Fernandez, Crawley et al 2025, eLife · CC BY 4.0

PMID 41031565
H&E stain of human brain autopsy tissue (formalin-fixed, paraffin-embedded) showing oligodendrocytes with the classic fried-egg appearance: round pale perinuclear halo from formalin fixation artefact, small dark nucleus. High magnification.

Jensflorian (Wikimedia Commons) · CC BY-SA 4.0

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