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α‐synuclein is developmentally expressed in cultured rat brain oligodendrocytes
Author(s) -
RichterLandsberg Christiane,
Gorath Michaela,
Trojanowski John Q.,
Lee Virginia M.Y.
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/1097-4547(20001001)62:1<9::aid-jnr2>3.0.co;2-u
Subject(s) - oligodendrocyte , biology , microbiology and biotechnology , cytoplasm , alpha (finance) , atrophy , immunofluorescence , in vitro , alpha synuclein , immunocytochemistry , white matter , neuroglia , neuroscience , central nervous system , pathology , immunology , myelin , endocrinology , antibody , parkinson's disease , genetics , psychology , medicine , clinical psychology , psychometrics , construct validity , magnetic resonance imaging , radiology , disease
Although a neuronal protein, α‐synuclein is a major component of glial cytoplasmic inclusions (GCIs) in oligodendrocytes of multiple system atrophy (MSA) brains. Because α‐synuclein has not been identified in oligodendrocytes of normal brains, we examined cultured rat brain oligodendrocytes during in vitro development and showed that α‐synuclein mRNA and protein are present in cultured oligodendrocytes. The expression of α‐synuclein was developmentally regulated; it increased to peak levels at 2 or 3 days in culture but declined thereafter. Indirect immunofluorescence further shows that α‐synuclein was localized predominantly in cell bodies and primary processes of oligodendroglia. Thus, GCIs may be a consequence of altered rather than de novo expression of α‐synuclein in MSA oligodendrocytes. J. Neurosci. Res. 62:9–14, 2000. © 2000 Wiley‐Liss, Inc.