ArticleDevelopment (Cambridge, England)2023
Gestational iron deficiency affects the ratio between interneuron subtypes in the postnatal cerebral cortex in mice.
Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Postnatal Iron Supplementation Fails to Fully Rescue Brain Metal and Transcriptional Defects Caused by Nutrition-Based Gestational Iron Deficiency.The Journal of nutrition · 2026Article
- Therapeutic hypothermia does not prevent dysmaturity of medial ganglionic eminence-derived interneurons in the dorsal hippocampus after neonatal hypoxia-ischemia.Experimental neurology · 2026Article
- Iron Deficiency Impairs Mitochondrial Energetics and Early Axonal Growth and Branching in Developing Hippocampal Neurons.The Journal of nutrition · 2026Article
- Chromatin accessibility and H3K9me3 landscapes reveal long-term epigenetic effects of fetal-neonatal iron deficiency in rat hippocampus.BMC genomics · 2024Article
- Integrating the dynamic and energetic fields of metabolism and development.Development (Cambridge, England) · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Gestational iron deficiency (gID) is highly prevalent and associated with an increased risk of intellectual and developmental disabilities in affected individuals that are often defined by a disrupted balance of excitation and inhibition (E/I) in the brain. Using a nutritional mouse model of gID, we previously demonstrated a shift in the E/I balance towards increased inhibition in the brains of gID offspring that was refractory to postnatal iron supplementation. We thus tested whether gID affects embryonic progenitor cells that are fated towards inhibitory interneurons. We quantified relevant cell populations during embryonic inhibitory neuron specification and found an increase in the proliferation of Nkx2.1+ interneuron progenitors in the embryonic medial ganglionic eminence at E14 that was associated with increased Shh signaling in gID animals at E12. When we quantified the number of mature inhibitory interneurons that are known to originate from the MGE, we found a persistent disruption of differentiated interneuron subtypes in early adulthood. Our data identify a cellular target that links gID with a disruption of cortical interneurons which play a major role in the establishment of the E/I balance.
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