Multimodal perspectives on the upper layer neurogenesis in the murine cerebral cortex

Upper layer corticogenesis provides mammals with a range of additional cognitive circuits. Through indirect neurogenesis, neuronal progenitor cells transition from radial glia cells to an intermediate stage, where they exponentially increase neuronal output, migrate into the upper regions of the neocortex, and settle as excitatory projection neurons. During this process, Glast1+ (Glutamate aspartate transporter 1) progenitor cells exit the cell cycle, begin to express NeuroD1 (Neuronal Differentiation 1), and irreversibly commit to a neuronal fate. The regulatory landscape governing the specific formation of the upper layers is not fully understood. In particular, the molecular mechanisms underlying the gradual transition of neurons into the post-mitotic state remain unresolved. A central question in this process is the influence of prenatal stressors on upper layer corticogenesis. In this study, we created a multimodal map of neurogenesis under both untreated and immune-activated conditions in a mouse model. Thereby, we monitored subtle canonical Wnt pathway-associated patterns that could explain the spontaneous aetiology of autism spectrum disorders or late-onset neurodegenerative diseases.