Radial glial cells, proliferating periventricular cells, and microglia might contribute to successful structural repair in the cerebral cortex of the lizard Gallotia galloti.
Reptiles are the only amniotic vertebrates known to be capable of spontaneous regeneration of the central nervous system (CNS). In this study, we analyzed the reactive changes of glial cells in response to a unilateral physical lesion in the cerebral cortex of the lizard Gallotia galloti, at 1, 3, 15, 30, 120, and 240 days postlesion. The glial cell markers glial fibrillary acidic protein (GFAP), glutamine synthetase (GS), S100 protein, and tomato lectin, as well as proliferating cell nuclear antigen (PCNA) were used to evaluate glial changes occurring because of cortical lesions. A transitory and unilateral upregulation of GFAP and GS in reactive radial glial cells were observed from 15 to 120 days postlesion. In addition, reactive lectin-positive macrophage/microglia were observed from 1 to 120 days postlesion, whereas the expression of S100 protein remained unchanged throughout the examined postlesion period. The matricial zones closest to the lesion site, the sulcus lateralis (SL) and the sulcus septomedialis (SSM), showed significantly increased numbers of dividing cells at 30 days postlesion. At 240 days postlesion, the staining pattern for PCNA, GFAP, GS, and tomato lectin in the lesion site became similar to that observed in unlesioned controls. In addition, ultrastructural data of the lesioned cortex at 240 days postlesion indicated a structural repair process. We conclude that restoration of the glial framework and generation of new neurons and glial cells in the ventricular wall play a key role in the successful structural repair of the cerebral cortex of the adult lizard.
Romero-Alemán
M M
MM
Departamento de Morfología (Biología Celular), Facultad de Ciencias de la Salud, Universidad de Las Palmas de Gran Canaria, 35080 Las Palmas, Canary Islands, Spain.
Monzón-Mayor
M
M
Yanes
C
C
Lang
D
D
D000818:Animals; D015415:Biomarkers; D001930:Brain Injuries / Q000378:metabolism / Q000503:physiopathology; D002454:Cell Differentiation / Q000502:physiology; D002455:Cell Division / Q000502:physiology; D002540:Cerebral Cortex / Q000254:growth & development* / Q000378:metabolism / Q000648:ultrastructure; D003714:Denervation; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism*; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism; D007150:Immunohistochemistry; D008116:Lizards / Q000033:anatomy & histology / Q000254:growth & development* / Q000378:metabolism; D017628:Microglia / Q000166:cytology / Q000378:metabolism; D009416:Nerve Regeneration / Q000502:physiology*; D009434:Neural Pathways / Q000378:metabolism / Q000648:ultrastructure; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000378:metabolism / Q000648:ultrastructure; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011930:Reaction Time / Q000502:physiology; D009418:S100 Proteins / Q000378:metabolism; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology
D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D018809:Proliferating Cell Nuclear Antigen; D009418:S100 Proteins; D005974:Glutamate-Ammonia Ligase