Publication: Microglial cells during the lesion-regeneration of the lizard medial cortex
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Date
1999
Authors
Nacher, J. ; Ramírez, G. ; Palop, J.J. ; Artal Soriano, Pablo ; Molowny, A. ; López-García, Carlos
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The lizard medial cortex (lizard fascia
dentata) is capable of neural regeneration after being
lesioned by the anti-metabolite 3-acetylpyridine (3AP).
This study was aimed at detecting microglial behaviour
during the medial cortex lesion-regeneration process
using tomato lectin histochemistry to label microglia
(both with light and electron microscopy) and
proliferating cell nuclear antigen (PCNA) immunocytochemistry
to label proliferating cells. As expected, 1-2
days post-injection lectin-labelled microglia cells could
not be observed in the medial cortex plexiform layers,
but later (7 days post-injection) abundant lectin-labelled
microglia cells re-populated the regenerating medial
cortex. Abundant PCNA-immunolabelled nuclei were
detected both in the subjacent ependymal neuroepithelium
(neuroblasts, maximum at 2 days postinjection)
as well as in some parenchyma1 cells which
were also lectin-labelled (microglia, maximum at 7-15
days post-injection). Re-invasive microglia were also
detected in the vicinity of ventricular ependymal lining,
blood vessels and meninges. The electron microscope
demonstrated that these microglial cells participate in
cell debris removal, especially of neural granular cell
somata. Other cell types related to microglia (mast cells,
peri-vascular cells and meningeal cells) were also
present during the scavenging process. Significant
numbers of microglial cells remained in close relationship
with the ependymal proliferative areas, even in
control non-lesioned animals. This is indirect evidence
for the working hypothesis that microglia are not only
implicated in cell debris removal, but also in the
regulation of newly generated neuroblast incorporation onto the cortical areas. Whether they phagocytose
immature neuroblasts or induce cell death in them or
even prevent their migration onto the principal layer
areas are likely possibilities that remain to be proven.
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