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Estradiol promotion of changes in the morphology of astroglia growing in culture depends on the expression of polysialic acid of neural membranes
Author(s) -
GarciaSegura Luis M.,
Cañas Benito,
Parducz Arpád,
Rougon Geneviève,
Theodosis Dionysia,
Naftolin Frederick,
TorresAleman Ignacio
Publication year - 1995
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.440130307
Subject(s) - polysialic acid , biology , glial fibrillary acidic protein , neural cell adhesion molecule , microbiology and biotechnology , immunostaining , cell culture , astrocyte , endocrinology , medicine , cell , central nervous system , biochemistry , cell adhesion , immunohistochemistry , immunology , genetics
Gonadal steroids are known to affect astroglial morphology in developing and adult animals. Earlier studies of mixed neuronal‐glial cultures from fetal rat hypothalamus showed that glial fibrillary acidic protein (GFAP)‐immunoreactive cells with a polygonal shape were transformed into process‐bearing cells upon exposure to the ovarian hormone estradiol. This effect was dependent on a direct contact of astroglia with living hypothalamic neurons. The present study shows that somata and processes of neurons in such cultures were immunoreactive for polysialic acid (PSA); astroglia were immunonegative. PSA appears to participate in the estradiol‐induced shape changes since treatment with endoneuraminidase, an enzyme that specifically removes PSA from the cell surface, abolished PSA immunostaining and prevented the 17ß‐estradiol‐induced morphological changes of astroglia. In contrast, treatment with endoneuraminidase did not affect astroglial shape changes induced by basic fibroblast growth factor (bFGF), nor those induced by the addition of neurons to glial cultures. These results suggest that PSA on neuronal membranes, probably linked to the highly sialylated isoform of the neural cell adhesion molecule, is necessary for the expression of certain hormonally‐regulated neuro‐glial interactions. © 1995 Wiley‐Liss, Inc.