Motor training compensates for cerebellar dysfunctions caused by oligodendrocyte ablation.
The role played by oligodendrocytes (OLs), the myelinating cells of the CNS, during brain development has not been fully explored. We have addressed this question by inducing a temporal and reversible ablation of OLs on postnatal CNS development. OL ablation in newborn mice leads to a profound alteration in the structure of the cerebellar cortex, which can be progressively rescued by newly generated cells, leading to a delayed myelination. Nevertheless, the temporal shift of the OL proliferation and myelinating program cannot completely compensate for developmental defects, resulting in impaired motor functions in the adult. Strikingly, we show that, despite these abnormalities, epigenetic factors, such as motor training, are able to fully rescue cerebellar-directed motor skills.
Collin
Ludovic
L
Institut de Génétique et de Biologie Moléculaire et Cellulaire, Department of Molecular Neurobiology, Universite Louis Pasteur, 1 Rue Laurent Fries, 67404 Illkirch Cedex, Communauté Urbaine de Strasbourg, France.
Usiello
Alessandro
A
Erbs
Eric
E
Mathis
Carole
C
Borrelli
Emiliana
E
D000818:Animals; D000831:Animals, Newborn; D002525:Cerebellar Cortex / Q000254:growth & development / Q000503:physiopathology* / Q000648:ultrastructure; D003711:Demyelinating Diseases / Q000503:physiopathology; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D008854:Microscopy, Electron; D009048:Motor Skills / Q000502:physiology*; D004676:Myelin Basic Protein / Q000235:genetics; D009186:Myelin Sheath / Q000502:physiology; D009836:Oligodendroglia / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D050683:R-SNARE Proteins; D013572:Synaptic Vesicles / Q000648:ultrastructure; D013937:Thymidine Kinase / Q000235:genetics
D008565:Membrane Proteins; D004676:Myelin Basic Protein; D050683:R-SNARE Proteins; D013937:Thymidine Kinase