ArticleScientific reports2017
Ephrin-A2 regulates excitatory neuron differentiation and interneuron migration in the developing neocortex.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Spatial transcriptomics reveals brain-wide circadian disruption in an Alzheimer's disease model.bioRxiv : the preprint server for biology · 2026Article
- Developmental regulation of long-range neuroblast migration by Eph/ephrin signaling.Frontiers in neuroscience · 2025Article
- Master regulators of neurogenesis: the dynamic roles of Ephrin receptors across diverse cellular niches.Translational psychiatry · 2024Review
- Aryl hydrocarbon receptor is a tumor promoter iniScience · 2023Article
- Identification of age-specific gene regulators of La Crosse virus neuroinvasion and pathogenesis.Nature communications · 2023Article
- Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review.Neurology and therapy · 2022Review
- Cortical interneuron function in autism spectrum condition.Pediatric research · 2019Review
- Identification of genes associated with cortical malformation using a transposon-mediated somatic mutagenesis screen in mice.Nature communications · 2018Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of the neocortex requires co-ordination between proliferation and differentiation, as well as the precise orchestration of neuronal migration. Eph/ephrin signaling is crucial in guiding neurons and their projections during embryonic development. In adult ephrin-A2 knockout mice we consistently observed focal patches of disorganized neocortical laminar architecture, ranging in severity from reduced neuronal density to a complete lack of neurons. Loss of ephrin-A2 in the pre-optic area of the diencephalon reduced the migration of neocortex-bound interneurons from this region. Furthermore, ephrin-A2 participates in the creation of excitatory neurons by inhibiting apical progenitor proliferation in the ventricular zone, with the disruption of ephrin-A2 signaling in these cells recapitulating the abnormal neocortex observed in the knockout. The disturbance to the architecture of the neocortex observed following deletion of ephrin-A2 signaling shares many similarities with defects found in the neocortex of children diagnosed with autism spectrum disorder.
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