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A study of in vitro and in vivo morphological changes of ependymal cells induced by galactocerebrosides
Author(s) -
Laabich Aicha,
Graff MarieNoëlle,
DunelErb Suzanne,
Sensenbrenner Monique,
Delaunoy JeanPierre
Publication year - 1991
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440040510
Subject(s) - ependymal cell , galactocerebroside , biology , ependyma , microbiology and biotechnology , in vivo , parenchyma , astrocyte , ultrastructure , pathology , anatomy , myelin , neuroscience , central nervous system , oligodendrocyte , medicine , botany
Ependymal cells in culture and in vivo were treated with mixture of galactocerebrosides. Galactocerebroside is the major glycolipid of myelin and in demyelinating diseases is found in cerebrospinal fluid. Morphological changes induced by this treatment were examined by microscopy at both optical and ultrastructural levels. In vitro, cilia, microvilli, and junctions between the cells disappeared, processes containing intermediate filaments developed, and the cells lost characteristics typical of ependymal cells and became more astrocyte‐like. As shown by vital staining with a fluorescent compound and by nuclear incorporation of bromodeoxyuridine, cells did not proliferate during the period of galactocerebroside treatment and the morphological transformation was restricted to the ependymal cells. In contrast, asialoganglioside‐GM 1 and sulfatides had no effect on ependymal cell morphology. Some of the in vitro observations could be reproduced in vivo. Junctions between ependymal cells disappeared and intercellular spaces appeared between these cells and the cerebral parenchyma at the basolateral side of the ependymal layer. At the apical side, morphological modifications of junctions and cilia were less evident. As these experimental conditions resemble those existing during demyelination the morphological changes described may account for perturbations of the physiological functions of the ependymal cell.