ArticleNeuroscience bulletin2024
Microglial EPOR Contribute to Sevoflurane-induced Developmental Fine Motor Deficits Through Synaptic Pruning in Mice.
Article in Neuroscience bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Neonatal Sevoflurane Exposure Induces Long-Term Cognitive Impairment via Epigenetically Mediated MMP9 Activation and Perineuronal Net Disruption in the Hippocampal CA2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Humanized Knock-in Mouse Model of the PSEN1 V97L Mutation from a Major Chinese Alzheimer's Disease Pedigree Reveals Early Neuroinflammation.Neuroscience bulletin · 2026Article
- Glycogen depletion in astrocytes induces sex-dimorphic remodeling of astrocytic and synaptic structures with concomitant anxiety-like behaviors and maternal care deficits.Biology of sex differences · 2025Article
- Ciprofol Alleviates Depressive-Like Behaviors in CUMS Mice Through PPARα-Associated ERK/CREB Signaling Activation.Drug design, development and therapy · 2025Article
- Therapeutic timing limitations of postnatal darbepoetin in a valproic acid rat model of Autism Spectrum Disorder.PloS one · 2025Article
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Authors and funding
12 authors.
Funding
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Abstract
Clinical researches including the Mayo Anesthesia Safety in Kids (MASK) study have found that children undergoing multiple anesthesia may have a higher risk of fine motor control difficulties. However, the underlying mechanisms remain elusive. Here, we report that erythropoietin receptor (EPOR), a microglial receptor associated with phagocytic activity, was significantly downregulated in the medial prefrontal cortex of young mice after multiple sevoflurane anesthesia exposure. Importantly, we found that the inhibited erythropoietin (EPO)/EPOR signaling axis led to microglial polarization, excessive excitatory synaptic pruning, and abnormal fine motor control skills in mice with multiple anesthesia exposure, and those above-mentioned situations were fully reversed by supplementing EPO-derived peptide ARA290 by intraperitoneal injection. Together, the microglial EPOR was identified as a key mediator regulating early synaptic development in this study, which impacted sevoflurane-induced fine motor dysfunction. Moreover, ARA290 might serve as a new treatment against neurotoxicity induced by general anesthesia in clinical practice by targeting the EPO/EPOR signaling pathway.
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