Motor learning promotes remyelination via new and surviving oligodendrocytes.

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Abstrakt

Tytuł:: Motor learning promotes remyelination via new and surviving oligodendrocytes.
Autorzy:: Bacmeister CM; Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.
Barr HJ; Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.
McClain CR; Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.
Thornton MA; Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.
Nettles D; Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.; Department of Neurosurgery, University of Colorado School of Medicine, Aurora, CO, USA.; Department of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, CO, USA.
Welle CG; Department of Neurosurgery, University of Colorado School of Medicine, Aurora, CO, USA.; Department of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, CO, USA.
Hughes EG; Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA. .
Źródło:: Nature neuroscience [Nat Neurosci] 2020 Jul; Vol. 23 (7), pp. 819-831. Date of Electronic Publication: 2020 May 18.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: <2002->: New York, NY : Nature Publishing Group
Original Publication: New York, NY : Nature America Inc., c1998-
MeSH Terms:: Learning/*physiology
Motor Activity/*physiology
Oligodendroglia/*physiology
Recovery of Function/*physiology
Remyelination/*physiology
Animals ; Cell Differentiation/physiology ; Cuprizone/toxicity ; Demyelinating Diseases/chemically induced ; Mice ; Mice, Inbred C57BL ; Monoamine Oxidase Inhibitors/toxicity ; Motor Cortex/physiology ; Oligodendrocyte Precursor Cells/physiology
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Grant Information:: T32 NS099042 United States NS NINDS NIH HHS; R21 NS106432 United States NS NINDS NIH HHS; P30 NS048154 United States NS NINDS NIH HHS; R01 NS086839 United States NS NINDS NIH HHS; R21 EY029458 United States EY NEI NIH HHS; R01 NS115975 United States NS NINDS NIH HHS
Substance Nomenclature:: 0 (Monoamine Oxidase Inhibitors)
5N16U7E0AO (Cuprizone)
Entry Date(s):: Date Created: 20200520 Date Completed: 20201007 Latest Revision: 20210518
Update Code:: 20240105
PubMed Central ID:: PMC7329620
DOI:: 10.1038/s41593-020-0637-3
PMID:: 32424285
: Czasopismo naukowe

Oligodendrocyte loss in neurological disease leaves axons vulnerable to damage and degeneration, and activity-dependent myelination may represent an endogenous mechanism to improve remyelination following injury. Here we report that, while learning a forelimb reach task transiently suppresses oligodendrogenesis, it subsequently increases oligodendrocyte precursor cell differentiation, oligodendrocyte generation and myelin sheath remodeling in the forelimb motor cortex. Immediately following demyelination, neurons exhibit hyperexcitability, learning is impaired and behavioral intervention provides no benefit to remyelination. However, partial remyelination restores neuronal and behavioral function, allowing learning to enhance oligodendrogenesis, remyelination of denuded axons and the ability of surviving oligodendrocytes to generate new myelin sheaths. Previously considered controversial, we show that sheath generation by mature oligodendrocytes is not only possible but also increases myelin pattern preservation following demyelination, thus presenting a new target for therapeutic interventions. Together, our findings demonstrate that precisely timed motor learning improves recovery from demyelinating injury via enhanced remyelination from new and surviving oligodendrocytes.

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