Abstract
How action potentials regulate myelination by oligodendrocytes is uncertain. We show that neuronal activity raises [Ca2+]i in developing oligodendrocytes in vivo and that myelin sheath elongation is promoted by a high frequency of [Ca2+]i transients and prevented by [Ca2+]i buffering. Sheath elongation occurs ~1 h after [Ca2+]i elevation. Sheath shortening is associated with a low frequency of [Ca2+]i transients but with longer duration [Ca2+]i bursts. Thus, [Ca2+]i controls myelin sheath development.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials / drug effects
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Action Potentials / genetics
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Animals
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Animals, Genetically Modified
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Axons / drug effects
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Axons / physiology*
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Calcium / metabolism*
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Calcium / pharmacology
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Chelating Agents / pharmacology
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Clustered Regularly Interspaced Short Palindromic Repeats
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Egtazic Acid / analogs & derivatives
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Egtazic Acid / pharmacology
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Luminescent Proteins / genetics
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Luminescent Proteins / metabolism
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Mivacurium / pharmacology
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Myelin Basic Protein / genetics
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Myelin Basic Protein / metabolism
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Myelin Sheath / physiology*
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Neuromuscular Nondepolarizing Agents / pharmacology
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Neurons / drug effects
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Neurons / physiology*
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Oligodendroglia / physiology*
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SOXE Transcription Factors / genetics
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SOXE Transcription Factors / metabolism
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Sodium Channel Blockers / pharmacology
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Spinal Cord / cytology
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Tetrodotoxin / pharmacology
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Zebrafish
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Zebrafish Proteins / genetics
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Zebrafish Proteins / metabolism
Substances
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Chelating Agents
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Luminescent Proteins
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Myelin Basic Protein
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Neuromuscular Nondepolarizing Agents
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SOXE Transcription Factors
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Sodium Channel Blockers
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Zebrafish Proteins
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sox10 protein, zebrafish
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Tetrodotoxin
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Egtazic Acid
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Mivacurium
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1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
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Calcium