Abstract
In human central nervous system (CNS) demyelinating diseases, spontaneous remyelination is often incomplete. Therefore, we have tested whether neutrotrophin-3 (NT-3) accelerates CNS myelin repair after a chemically-induced demyelination. One group of adult rats was injected in the corpus callosum (CC) with 1 microl of 1% lysophosphatidylcholine (LPC) and 1 microl of NT-3 (1 microg/microl), and 15 days after injury (D15) remyelination was compared to control rats (receiving 1 microl of LPC+1 microl of vehicle buffer of NT-3). The demyelinated volume decreased by 56% in NT-3-treated rats at D15, and immunohistochemistry showed an increase in mature MBP(+) oligodendrocytes (OL) (+66%) in treated animals (whereas less mature (CNP(+)) OL were unchanged). Since less than 3% axons degenerate in this model, and as astrocytic gliosis was not modified, these data suggest that NT-3 acts directly on cells of the OL lineage to enhance remyelination in vivo.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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2',3'-Cyclic-Nucleotide Phosphodiesterases / metabolism
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Animals
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Bromodeoxyuridine / metabolism
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Central Nervous System Diseases / pathology
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Central Nervous System Diseases / physiopathology
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Corpus Callosum / drug effects
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Corpus Callosum / pathology
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Demyelinating Diseases / chemically induced
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Demyelinating Diseases / pathology*
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Demyelinating Diseases / physiopathology
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Disease Models, Animal
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Glial Fibrillary Acidic Protein / metabolism
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Immunohistochemistry
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Lysophosphatidylcholines / toxicity
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Male
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Myelin Basic Protein / metabolism
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Nerve Regeneration / physiology*
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Neurotrophin 3 / pharmacology*
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Oligodendroglia / drug effects*
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Oligodendroglia / metabolism
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Rats
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Rats, Wistar
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Stem Cells / metabolism
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Time Factors
Substances
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Glial Fibrillary Acidic Protein
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Lysophosphatidylcholines
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Myelin Basic Protein
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Neurotrophin 3
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2',3'-Cyclic-Nucleotide Phosphodiesterases
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Bromodeoxyuridine