Retinal Ganglion Cell Loss and Microglial Activation in a SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis

The neurodegenerative disease amyotrophic lateral sclerosis (ALS) affects the spinal cord, brain stem, and cerebral cortex. In this pathology, both neurons and glial cells are affected. However, few studies have analyzed retinal microglia in ALS models. In this study, we quantified the signs of micr...

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Detalles Bibliográficos
Autores: Rojas Lozano, María Del Pilar, Ramírez Sebastián, Ana Isabel, Cadena Santoyo, Manuel, Fernández Arrabal, José Antonio, García Martín, Elena Salobrar, López Cuenca, Inés, Santos García, Irene, Lago Femia, Eva De, Urcelay Segura, José Luis, Ramírez Sebastián, José Manuel, Hoz Montañana, María Rosa De, Salazar Corral, Juan José
Tipo de recurso: artículo
Fecha de publicación:2021
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/7792
Acceso en línea:https://hdl.handle.net/20.500.14352/7792
Access Level:acceso abierto
Palabra clave:611.8.018.24:617.735
616.832.522:617.735-007
Microglia
Retina
SOD1G93A mouse model
ALS
Retinal whole-mount
Microglial activation
Retinal ganglion cells
Pro-inflammatory M1 phenotype
Anti-inflammatory M2 phenotype
Neurociencias (Medicina)
Oftalmología
Anatomía ocular
2490 Neurociencias
3201.09 Oftalmología
Descripción
Sumario:The neurodegenerative disease amyotrophic lateral sclerosis (ALS) affects the spinal cord, brain stem, and cerebral cortex. In this pathology, both neurons and glial cells are affected. However, few studies have analyzed retinal microglia in ALS models. In this study, we quantified the signs of microglial activation and the number of retinal ganglion cells (RGCs) in an SOD1G93A transgenic mouse model at 120 days (advanced stage of the disease) in retinal whole-mounts. For SOD1G93A animals (compared to the wild-type), we found, in microglial cells, (i) a significant increase in the area occupied by each microglial cell in the total area of the retina; (ii) a significant increase in the arbor area in the outer plexiform layer (OPL) inferior sector; (iii) the presence of cells with retracted processes; (iv) areas of cell groupings in some sectors; (v) no significant increase in the number of microglial cells; (vi) the expression of IFN-γ and IL-1β; and (vii) the non-expression of IL-10 and arginase-I. For the RGCs, we found a decrease in their number. In conclusion, in the SOD1G93A model (at 120 days), retinal microglial activation occurred, taking a pro-inflammatory phenotype M1, which affected the OPL and inner retinal layers and could be related to RGC loss