Microglial cells during the lesion-regeneration of the lizard medial cortex


  • C. López García
  • J. Nacher
  • C. Ramírez
  • J. J. Palop
  • P. Artal
  • A. Molowny


phagocytosis, tomato lectin histochemistry, ultrastructure, hippocampus, 3-acetylpyrydine


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.