The myelination is a critical process during brain development. This study aimed to explore the impact of volatile anesthetic sevoflurane on developing myelination and the role of microglial activation in this process. Neonatal C57BL/6J mice were exposed to sevoflurane at their postnatal 6-8 days. Neurobehavioral tests were used to assess fine motor and cognitive functions. Myelination of hippocampus (HC) and corpus callosum (CC), as well as microglial activation, were determined by western blotting and immunostaining. Lipid droplets were assessed by Oil-Red-O and Bodipy staining. Further, primary microglia were co-cultured with oligodendrocyte precursor cell (OPC) to determine the role of microglia in the proliferation and differentiation of OPC. And microglial inhibitor minocycline and CSF1R inhibitor PLX5622 were administered to assess the effects of microglial activation on developing myelination. The results showed that repeated sevoflurane exposure impaired both fine motor and cognitive functions and induced abnormal expressions of myelin-related proteins myelin basic protein (MBP) and platelet-derived growth factor α receptor (PDGFR-α). And accumulations of lipid droplets were found in the microglia of HC and CC after sevoflurane exposure. Further, the spatiotemporal response to repeated sevoflurane exposure in glial cells exhibited an aberrant myelination process and microglial polarization. The conditioned medium from sevoflurane-treated microglia inhibited the OPC proliferation and differentiation, while minocycline or PLX5622 alleviated sevoflurane-induced neuroinflammation and hypomyelination. Therefore, repeated sevoflurane exposure negatively affected OPC differentiation and myelination trajectory through hyperactivating microglia in developing brain, leading to motor and cognitive impairments, while microglial inhibition/depletion could protect against sevoflurane-induced damage on developing myelination.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/glia.70000 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Corrigendum to "Enriched environment mitigates cognitive impairment in pre-adolescent mice following repeated neonatal sevoflurane exposure by reducing TTBK1 expression and Tau phosphorylation" [Neuropharmacology 268 (2025) 110327].
Neuropharmacology
February 2025
Department of Anesthesia, Tianjin Medical University General Hospital, PR China; Tianjin Institute of Anesthesiology, Tianjin, 300052, PR China. Electronic address:
Histone lactylation protects against sevoflurane-induced cognitive impairment by regulating YTHDF3/PRDX3 mediated microglial pyroptosis in neonatal mice.
Int Immunopharmacol
April 2025
Department of Anesthesiology, The First Affiliated Hospital of Soochow University, Suzhou 215006 Jiangsu Province, PR China; Institute of Anesthesiology, Soochow University, Suzhou 215006 Jiangsu Province, PR China. Electronic address:
Background: Sevoflurane (SEV), a widely used inhalational anesthetic, multiple SEV exposures has been implicated in cognitive impairment, particularly in neonates. However, the mechanisms underlying SEV-induced cognitive impairment not fully understood.
Methods: Neonatal mice or murine microglial line BV-2 cells were exposed to SEV.
MicroRNA-197-3p Transfection: Variations in Cardiomyocyte Gene Expression with Anaesthetics Drugs in a Model of Hypoxia/Reperfusion.
Pharmaceuticals (Basel)
January 2025
Institute of Biomedical Research in Malaga, 29010 Malaga, Spain.
Our research team analyzed the microRNA (miRNA)-197-3p involved in cardioprotection, and we demonstrated that the overexpression of miRNA-197-3p could be linked to a higher risk of cardiac damage. Recent research indicated that miRNA-197-3p inhibits the effector proteins of the anaesthetic preconditioning mechanism of halogenated drugs. In this scenario, we proposed to determine the role of miRNA-197-3p in cardiac injury and its effects on myocardial conditioning under halogenated exposure.
View Article and Find Full Text PDFMicroglial pyroptosis induced by SENP7 via the cGAS/STING/IRF3 pathway contributes to neuronal apoptosis.
Cytokine
February 2025
Department of Reproductive Medicine Center, Jiaxing Maternity and Child Health Care Hospital, Jiaxing Women and Children's Hospital, Wenzhou Medical University, Jiaxing 314050, Zhejiang, PR China.
Background: Maternal anesthetic exposure may exacerbate significant neurocognitive risks in the immature brains of fetuses. However, the mechanisms through which sevoflurane exposure during pregnancy results in cognitive impairments in offspring remain unclear.
Methods: Pregnant C57BL/6 mice (gestational day 14) were intervented with 2.
Nrf2 Ameliorates Sevoflurane-Induced Cognitive Deficits in Aged Mice by Inhibiting Neuroinflammation in the Hippocampus.
Mol Neurobiol
February 2025
Department of Anesthesiology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, No. 107 Yanjiang West Road, Guangzhou, 510120, China.
Perioperative neurocognitive disorders (PND), common complications that occur after anesthetized surgery in elderly patients, are major challenges to our rapidly growing aging population. The transcription factor known as nuclear factor erythroid-2-related factor 2 (Nrf2) is an essential component of the cellular antioxidant response, purportedly contributing to the preservation of cognitive functions such as learning and memory. Nevertheless, the function and intracellular processes involving Nrf2 in PND remain largely unknown.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!