ArticleFrontiers in pharmacology2022
Maternal sevoflurane exposure induces neurotoxicity in offspring rats
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Developmental stage-dependent neurotoxicity of sevoflurane: evidence from brain organoids.Frontiers in cellular neuroscience · 2026Review
- Dexmedetomidine Improves Long-term Neurological Outcomes by Promoting Oligodendrocyte Genesis and Myelination in Neonatal Rats Following Hypoxic-ischemic Brain Injury.Molecular neurobiology · 2025Article
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4 authors at 1 institution in 1 country.
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Abstract
Sevoflurane is widely used for maternal anesthesia during pregnancy. Sevoflurane exposure of rats at mid-gestation can cause abnormal development of the central nervous system in their offspring. Sevoflurane is known to increase the expression of cannabinoid 1 receptor (CB1R) in the hippocampus. However, the effect of cannabinoid 1 receptor on fetal and offspring rats after maternal anesthesia is still unclear. At gestational day 14, pregnant rats were subjected to 2-h exposure to 3.5% sevoflurane or air. Rats underwent intraperitoneal injection with saline or rimonabant (1 mg/kg) 30 min prior to sevoflurane or air exposure. cannabinoid 1 receptor, cyclin-dependent kinase 5 (CDK5), p35, p25, tau, and p-tau expression in fetal brains was measured at 6, 12, and 24 h post-sevoflurane/air exposure. Neurobehavioral and Morris water maze tests were performed postnatal days 3-33. The expression of cannabinoid 1 receptor/cyclin-dependent kinase 5/p-tau and histopathological staining of brain tissues in offspring rats was observed. We found that a single exposure to sevoflurane upregulated the activity of cyclin-dependent kinase 5 and the level of p-tau
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