Myelin replacement triggered by single-cell demyelination in mouse cortex

Nicolas Snaidero (), Martina Schifferer, Aleksandra Mezydlo, Bernard Zalc, Martin Kerschensteiner and Thomas Misgeld
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Nicolas Snaidero: Institute of Neuronal Cell Biology, Technische Universität München
Martina Schifferer: German Center for Neurodegenerative Diseases (DZNE)
Aleksandra Mezydlo: University Hospital, Ludwig-Maximilians Universität München
Bernard Zalc: Inserm, CNRS, Institut du Cerveau, Pitié-Salpêtrière Hospital, Sorbonne Université
Martin Kerschensteiner: University Hospital, Ludwig-Maximilians Universität München
Thomas Misgeld: Institute of Neuronal Cell Biology, Technische Universität München

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract Myelin, rather than being a static insulator of axons, is emerging as an active participant in circuit plasticity. This requires precise regulation of oligodendrocyte numbers and myelination patterns. Here, by devising a laser ablation approach of single oligodendrocytes, followed by in vivo imaging and correlated ultrastructural reconstructions, we report that in mouse cortex demyelination as subtle as the loss of a single oligodendrocyte can trigger robust cell replacement and remyelination timed by myelin breakdown. This results in reliable reestablishment of the original myelin pattern along continuously myelinated axons, while in parallel, patchy isolated internodes emerge on previously unmyelinated axons. Therefore, in mammalian cortex, internodes along partially myelinated cortical axons are typically not reestablished, suggesting that the cues that guide patchy myelination are not preserved through cycles of de- and remyelination. In contrast, myelin sheaths forming continuous patterns show remarkable homeostatic resilience and remyelinate with single axon precision.

Date: 2020
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DOI: 10.1038/s41467-020-18632-0

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