RESUMEN
The mechanisms governing the expansion of neuron number in specific brain regions are still poorly understood. Enlarged neuron numbers in different species are often anticipated by increased numbers of progenitors dividing in the subventricular zone. Here we present live imaging analysis of radial glial cells and their progeny in the ventral telencephalon, the region with the largest subventricular zone in the murine brain during neurogenesis. We observe lineage amplification by a new type of progenitor, including bipolar radial glial cells dividing at subapical positions and generating further proliferating progeny. The frequency of this new type of progenitor is increased not only in larger clones of the mouse lateral ganglionic eminence but also in cerebral cortices of gyrated species, and upon inducing gyrification in the murine cerebral cortex. This implies key roles of this new type of radial glia in ontogeny and phylogeny.
Asunto(s)
Células Ependimogliales/citología , Células-Madre Neurales/citología , Neurogénesis , Neuronas/citología , Telencéfalo/citología , Animales , Diferenciación Celular , Linaje de la Célula/fisiología , Proliferación Celular , Embrión de Mamíferos , Células Ependimogliales/metabolismo , Genes Reporteros , Proteínas Fluorescentes Verdes , Ratones , Ratones Transgénicos , Células-Madre Neurales/metabolismo , Neuronas/metabolismo , Telencéfalo/embriología , Telencéfalo/metabolismo , Imagen de Lapso de Tiempo , Técnicas de Cultivo de TejidosRESUMEN
Astrocytes are thought to have important roles after brain injury, but their behavior has largely been inferred from postmortem analysis. To examine the mechanisms that recruit astrocytes to sites of injury, we used in vivo two-photon laser-scanning microscopy to follow the response of GFP-labeled astrocytes in the adult mouse cerebral cortex over several weeks after acute injury. Live imaging revealed a marked heterogeneity in the reaction of individual astrocytes, with one subset retaining their initial morphology, another directing their processes toward the lesion, and a distinct subset located at juxtavascular sites proliferating. Although no astrocytes actively migrated toward the injury site, selective proliferation of juxtavascular astrocytes was observed after the introduction of a lesion and was still the case, even though the extent was reduced, after astrocyte-specific deletion of the RhoGTPase Cdc42. Thus, astrocyte recruitment after injury relies solely on proliferation in a specific niche.
