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Galactocerebroside and sulfatide independently mediate Ca 2+ responses in oligodendrocytes
Author(s) -
Dyer C. A.,
Benjamins J. A.
Publication year - 1991
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/jnr.490300414
Subject(s) - galactocerebroside , myelin , oligodendrocyte , microbiology and biotechnology , antibody , myelin oligodendrocyte glycoprotein , sphingolipid , chemistry , biology , immunology , neuroscience , central nervous system
Galactocerebroside (GalC) and sulfated galactocerebroside (sulfatide) are sphingolipids highly enriched in myelin. The binding of antibodies reactive with either sulfatide Or GalC to cultured Oligodendrocytes causes a Ca 2+ influx, followed by microtubule depo lymerization; however, antisulfatide is less effective than anti‐GalC in altering cytoskeleton. Typical Ca 2+ responses are delayed for both antibodies but are transient for sulfatide‐reactive antibodies in contrast to the sustained responses previously reported for anti‐GalC (Dyer and Benjamins, J Cell Biol 111:625–633, 1990). Approximately one‐half as many oligodendrocytes respond to sulfatide‐reactive antibodies (about 39%) as to anti‐GalC (about 75%). Subpopulations of Oligodendrocytes were identified that responded to neither antibody, only one antibody, or both antibodies, indicating that sulfatide and GalC independently mediate Ca2 2+ responses. These results suggest that sulfatide and GalC have different physiologic roles in regulating elaboration of myelin membrane by oligodendrocytes in vivo and support the possibility that viral or immune attack via GalC or sulfatide on oligodendrocytes may mimic normal signals in a manner that disrupts the sequence of events that coordinates myelination or maintenance of myelin in vivo.