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Journal of Neuroscience, Vol 12, 872-882, Copyright © 1992 by Society for Neuroscience
The embryonic form of neural cell surface molecule (E-NCAM) in the rat hippocampus and its reexpression on glial cells following kainic acid- induced status epilepticus
G Le Gal La Salle, G Rougon and A Valin
Departement de Neuroanatomie Fonctionnelle, CNRS, Gif sur Yvette, France.
The neural cell adhesion molecule (NCAM) changes at the cell surface during
development, from highly sialylated forms (embryonic or E-NCAM) to three
size classes of less sialylated proteins with apparent molecular mass of
180, 140, and 120 kDa (adult NCAM). In the nervous system, E-NCAM has been
localized in developing tissues, where it is thought to play a role in the
structuring of neuronal groups and tissue pattern formation. In the present
study a monoclonal antibody that specifically detects E-NCAM was used in
immunoblot and immunohistochemical procedures. In developing rat
hippocampus, E-NCAM cell expression was found to change according to a
precise pattern and persisted until 1 month after birth. It was closely
associated with the mossy fiber system, an area known for its sprouting
propensity. In adult rats, although immunoreactivity considerably decreases
and becomes undetectable by immunoblot analysis, E-NCAM was still found to
be associated with a few pyramidal-shaped cells in the innermost part of
the dentate gyrus. In order to acquire some insight into potential
histogenetically plastic functions of E-NCAM, in another series of
experiments adult rats were treated with kainic acid, a powerful
excitotoxic and convulsant glutamate analog eliciting status epilepticus.
When these animals were examined for E-NCAM expression, an intense labeling
was found associated with glial-like cells, particularly in the hippocampal
formation, and corresponding approximately to the reactive gliosis, as
confirmed by staining with anti-glial fibrillary acidic protein antibodies.
This expression was detectable from about 3 d following kainic acid
administration and persisted for at least 12 weeks; it developed according
to an observable spatiotemporal distribution pattern. In animals submitted
to amygdala kindling, a nonlesional model of secondarily generalized
epilepsy, no such reexpression of E-NCAM was observed. Our observations
imply that polysialylation may be a means of identifying neuronal
structures capable of plasticity in the CNS. Moreover, intense reexpression
of E-NCAM could be a marker of reactive gliosis following brain damage.
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