Journal
SCIENCE
Volume 344, Issue 6183, Pages 487-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1252304
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Funding
- National Institute of Neurological Disorders and Stroke [NINDS K08NS070926, R01 EY10257]
- California Institute for Regenerative Medicine [CIRM RB4-06093, RN3-06510]
- Alex's Lemonade Stand Foundation
- McKenna Claire Foundation
- Cure Starts Now
- Lyla Nsouli Foundation
- Dylan Jewett Fund
- Connor Johnson Fund
- Zoey Ganesh Fund
- Dylan Frick Fund
- Abigail Jensen Fund
- Wayland Villars Fund
- Jennifer Kranz Memorial Fund
- Ludwig Foundation
- Price Family Charitable Fund
- Stanford Medical Scientist Training Program
- Stanford Institute for Neuro-Innovation and Translational Neurosciences
- Child Health Research Institute
- Lucile Packard Foundation for Children's Health, Stanford University Clinical & Translation Science Award [UL1 RR025744]
- Howard Hughes Medical Institute Fellowship of the Life Sciences Research Foundation
- Bezos Family Foundation
- Child Health Research Institute at Stanford University, Anne T. and Robert M. Bass Endowed Faculty Scholarship in Pediatric Cancer and Blood Diseases
- NIH [1S10RR02678001]
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Myelination of the central nervous system requires the generation of functionally mature oligodendrocytes from oligodendrocyte precursor cells (OPCs). Electrically active neurons may influence OPC function and selectively instruct myelination of an active neural circuit. In this work, we use optogenetic stimulation of the premotor cortex in awake, behaving mice to demonstrate that neuronal activity elicits a mitogenic response of neural progenitor cells and OPCs, promotes oligodendrogenesis, and increases myelination within the deep layers of the premotor cortex and subcortical white matter. We further show that this neuronal activity-regulated oligodendrogenesis and myelination is associated with improved motor function of the corresponding limb. Oligodendrogenesis and myelination appear necessary for the observed functional improvement, as epigenetic blockade of oligodendrocyte differentiation and myelin changes prevents the activity-regulated behavioral improvement.
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