White Matter Plasticity and Enhanced Remyelination in the Maternal CNS

White Matter Plasticity and Enhanced Remyelination in the Maternal CNS

Myelination, the process in which oligodendrocytes coat CNS axons with a myelin sheath, represents an important but poorly understood form of neural plasticity that may be sexually dimorphic in the adult CNS. Remission of multiple sclerosis during pregnancy led us to hypothesize that remyelination i...

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Bibliographic Details
Published in:The Journal of neuroscience Vol. 27; no. 8; pp. 1812 - 1823
Main Authors: Gregg, Christopher, Shikar, Viktor, Larsen, Peter, Mak, Gloria, Chojnacki, Andrew, Yong, V. Wee, Weiss, Samuel
Format: Journal Article
Language:English
Published: United States Soc Neuroscience 21-02-2007
Society for Neuroscience
Subjects:
Animals
Cell Division
Cell Proliferation
Cells, Cultured
Central Nervous System - cytology
Central Nervous System - physiology
Female
Mice
Mice, Inbred Strains
Myelin Sheath - physiology
Nerve Regeneration - drug effects
Nerve Regeneration - physiology
Neuronal Plasticity - physiology
Oligodendroglia - cytology
Postpartum Period - physiology
Pregnancy
Pregnancy, Animal - physiology
Prolactin - metabolism
Prolactin - pharmacology
Signal Transduction - physiology
Stem Cells - cytology
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Summary:Myelination, the process in which oligodendrocytes coat CNS axons with a myelin sheath, represents an important but poorly understood form of neural plasticity that may be sexually dimorphic in the adult CNS. Remission of multiple sclerosis during pregnancy led us to hypothesize that remyelination is enhanced in the maternal brain. Here we report an increase in the generation of myelin-forming oligodendrocytes and in the number of myelinated axons in the maternal murine CNS. Remarkably, pregnant mice have an enhanced ability to remyelinate white matter lesions. The hormone prolactin regulates oligodendrocyte precursor proliferation and mimics the regenerative effects of pregnancy. This suggests that maternal white matter plasticity imparts a striking ability to repair demyelination and identifies prolactin as a potential therapeutic agent.
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ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.4441-06.2007