ArticleNature communications2019
Developmental cell death regulates lineage-related interneuron-oligodendroglia functional clusters and oligodendrocyte homeostasis.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 74 citations in OpenAlex.
- Linking neurogenesis, oligodendrogenesis, and myelination defects to neurodevelopmental disruption in primary mitochondrial disorders.FEBS letters · 2026Review
- Prefrontal gamma oscillations and fear extinction learning require early postnatal interneuron-oligodendroglia communication.Nature communications · 2025Article
- Human oligodendrocyte progenitor cells mediate synapse elimination through TAM receptor activation.Nature communications · 2025Article
- Oligodendrocyte lineage cells dysfunction in depression: early life stress, adolescent vulnerability and the emerging role of lipid metabolism.Translational psychiatry · 2025Review
- Review
- Prenatal valproic acid on the basis of gestational diabetes also induces autistic behavior and disrupts myelination and oligodendroglial maturation slightly in offspring.Translational psychiatry · 2025Article
- Article
- Embryonic origins of forebrain oligodendrocytes revisited by combinatorial genetic fate mapping.eLife · 2024Article
- Interaction between Oligodendrocytes and Interneurons in Brain Development and Related Neuropsychiatric Disorders.International journal of molecular sciences · 2024Review
- Features, Fates, and Functions of Oligodendrocyte Precursor Cells.Cold Spring Harbor perspectives in biology · 2024Review
- Glial modulation of synapse development and plasticity: oligodendrocyte precursor cells as a new player in the synaptic quintet.Frontiers in cell and developmental biology · 2024Review
- Physiological features of parvalbumin-expressing GABAergic interneurons contributing to high-frequency oscillations in the cerebral cortex.Current research in neurobiology · 2024Review
- Psychiatric risk gene Transcription Factor 4 (TCF4) regulates the density and connectivity of distinct inhibitory interneuron subtypes.Molecular psychiatry · 2023Article
- Oligodendrocyte precursor cells: the multitaskers in the brain.Pflugers Archiv : European journal of physiology · 2023Review
- Impact of Developmental Changes of GABAInternational journal of molecular sciences · 2023Article
- Emerging mitochondrial-mediated mechanisms involved in oligodendrocyte development.Journal of neuroscience research · 2023Review
- The roles of microglia and astrocytes in myelin phagocytosis in the central nervous system.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Utilizing hiPSC-derived oligodendrocytes to study myelin pathophysiology in neuropsychiatric and neurodegenerative disorders.Frontiers in cellular neuroscience · 2023Review
- Neuron-glia crosstalk shapes brain morphogenesis.Clinical and translational medicine · 2022Article
- Evidence for oligodendrocyte progenitor cell heterogeneity in the adult mouse brain.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The first wave of oligodendrocyte precursor cells (firstOPCs) and most GABAergic interneurons share common embryonic origins. Cortical firstOPCs are thought to be replaced by other OPC populations shortly after birth, maintaining a consistent OPC density and making postnatal interactions between firstOPCs and ontogenetically-related interneurons unlikely. Challenging these ideas, we show that a cortical firstOPC subpopulation survives and forms functional cell clusters with lineage-related interneurons. Favored by a common embryonic origin, these clusters display unexpected preferential synaptic connectivity and are anatomically maintained after firstOPCs differentiate into myelinating oligodendrocytes. While the concomitant rescue of interneurons and firstOPCs committed to die causes an exacerbated neuronal inhibition, it abolishes interneuron-firstOPC high synaptic connectivity. Further, the number of other oligodendroglia populations increases through a non-cell-autonomous mechanism, impacting myelination. These findings demonstrate unprecedented roles of interneuron and firstOPC apoptosis in regulating lineage-related cell interactions and the homeostatic oligodendroglia density.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.