ArticleNature communications2024
Developmental Cajal-Retzius cell death contributes to the maturation of layer 1 cortical inhibition and somatosensory processing.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Network integration of neocortical Cajal-Retzius neurons shapes early cortical dynamics and contributes to their transient nature.Cell communication and signaling : CCS · 2026Article
- Scalable single-cell total RNA sequencing unifies coding and noncoding transcriptomics.Nature biotechnology · 2026Article
- Differences in Cajal-Retzius Cell Density and Postnatal Persistence Across Cortical Areas Revealed by a Novel Intersectional Genetic Labeling Approach.The Journal of comparative neurology · 2025Article
- Scalable single-cell total RNA-seq reveals non-coding programs in immunity, infection, and brain development.Research square · 2025Article
- Loss of Postnatal Retinal Input Perturbs Cortical Lamination in the Developing Ferret Visual Cortex.The Journal of comparative neurology · 2025Article
- Development of spontaneous and sensory evoked network activity in rodent cerebral cortexFrontiers in cellular neuroscience · 2025Review
- GABAergic integration of transient and persistent neurons in the developing mouse somatosensory cortex.Frontiers in cellular neuroscience · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
The role of developmental cell death in the formation of brain circuits is not well understood. Cajal-Retzius cells constitute a major transient neuronal population in the mammalian neocortex, which largely disappears at the time of postnatal somatosensory maturation. In this study, we used mouse genetics, anatomical, functional, and behavioral approaches to explore the impact of the early postnatal death of Cajal-Retzius cells in the maturation of the cortical circuit. We find that before their death, Cajal-Retzius cells mainly receive inputs from layer 1 neurons, which can only develop their mature connectivity onto layer 2/3 pyramidal cells after Cajal-Retzius cells disappear. This developmental connectivity progression from layer 1 GABAergic to layer 2/3 pyramidal cells regulates sensory-driven inhibition within, and more so, across cortical columns. Here we show that Cajal-Retzius cell death prevention leads to layer 2/3 hyper-excitability, delayed learning and reduced performance in a multi-whisker-dependent texture discrimination task.
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