ArticlePLoS biology2019
Astroglial dysfunctions drive aberrant synaptogenesis and social behavioral deficits in mice with neonatal exposure to lengthy general anesthesia.
Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 89 citations in OpenAlex.
- Sevoflurane-induced disruption of critical period Arc signaling drives aberrant microglial synaptic pruning and cognitive deficits.Acta pharmacologica Sinica · 2026Article
- Astrocyte TrkB.T1 Deficiency Disrupts Glutamatergic Synaptogenesis and Astrocyte-Synapse Interactions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Dual adeno-associated virus system for selective and sparse labeling of astrocytes.Neural regeneration research · 2026Article
- Environmental enrichment mitigates sevoflurane-induced neurodevelopmental injury via cGAS-STING-dependent microglial modulation.Cell & bioscience · 2026Article
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- State-Dependent Remodeling of Astrocytic Proteome and Phosphorylation Signaling Networks Across Wake, Sleep, and General Anesthesia.International journal of molecular sciences · 2026Article
- Astrocyte Ezrin defines resilience to stress-induced depressive behaviours in mice.National science review · 2026Article
- Therapeutic Values of General Anesthetics: From Developmental Neurotoxicity to Neurotherapeutic Agents.Current neuropharmacology · 2026Review
- Glymphatic-meningeal lymphatic system imbalance: a peripheral-to-central inflammatory bridge in perioperative neurocognitive disorders.Frontiers in immunology · 2026Review
- Rutin ameliorates sevoflurane-induced neurotoxicity by inhibiting microglial synaptic phagocytosis through the complement pathway.Scientific reports · 2025Article
- Astrocyte morphological remodeling regulates consciousness state transitions induced by inhaled general anesthesia.Molecular psychiatry · 2025Article
- From neurotoxicity to neuroprotection: Rethinking GABACell biology and toxicology · 2025Review
- Human neuron chimeric mice reveal impairment of DVL-1-mediated neuronal migration by sevoflurane and potential treatment by rTMS.Experimental & molecular medicine · 2025Article
- From initial formation to developmental refinement: GABAergic inputs shape neuronal subnetworks in the primary somatosensory cortex.iScience · 2025Article
- Role of glia in delirium: proposed mechanisms and translational implications.Molecular psychiatry · 2025Review
- The Relationship between Early Exposure to General Anesthesia and Neurobehavioral Deficits.Developmental neuroscience · 2025Review
- Astrocyte morphology.Trends in cell biology · 2024Review
- General anesthetic agents induce neurotoxicity through oligodendrocytes in the developing brain.Zoological research · 2024Review
- Integrated ribosome and proteome analyses reveal insights into sevoflurane-induced long-term social behavior and cognitive dysfunctions through ADNP inhibition in neonatal mice.Zoological research · 2024Article
- Complement C1q-mediated microglial synaptic elimination by enhancing desialylation underlies sevoflurane-induced developmental neurotoxicity.Cell & bioscience · 2024Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lengthy use of general anesthetics (GAs) causes neurobehavioral deficits in the developing brain, which has raised significant clinical concerns such that the United States Food and Drug Administration (FDA) is warning on the use of GAs in children younger than 3 years. However, the molecular and cellular mechanisms for GAs-induced neurotoxicity remain largely unknown. Here, we report that sevoflurane (Sevo), a commonly used GA in pediatrics, caused compromised astrocyte morphogenesis spatiotemporally correlated to synaptic overgrowth, with reduced synaptic function in developing cortex in a regional-, exposure-length-, and age-specific manner. Sevo disrupted astrocyte Ca2+ homeostasis both acutely and chronically, which led to the down-regulation of Ezrin, an actin-binding membrane-bound protein, which we found was critically involved in astrocyte morphogenesis in vivo. Importantly, overexpression of astrocyte Ezrin rescued astrocytic and neuronal dysfunctions and fully corrected deficits in social behaviors in developing mice with lengthy Sevo exposure. Our data uncover that, in addition to neurons, astrocytes may represent important targets for GAs to exert toxic effects and that astrocyte morphological integrity is crucial for synaptogenesis and neurological behaviors.
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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.