ArticleMolecular neurobiology2017
Repeated Neonatal Sevoflurane Exposure-Induced Developmental Delays of Parvalbumin Interneurons and Cognitive Impairments Are Reversed by Environmental Enrichment.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Environmental enrichment modulates parvalbumin interneuron deficits and plasticity-related signaling after early postnatal NMDA receptor hypofunction in male rat visual cortex.Brain structure & function · 2026Article
- Sevoflurane versus propofol and the long-term risk of attention-deficit/hyperactivity disorder in children.General psychiatry · 2026Article
- Therapeutic Values of General Anesthetics: From Developmental Neurotoxicity to Neurotherapeutic Agents.Current neuropharmacology · 2026Review
- Restricted Daily Exposure of Environmental Enrichment: Bridging the Practical Gap from Animal Studies to Human Application.International journal of environmental research and public health · 2024Review
- Translatome and transcriptome profiling of neonatal mice hippocampus exposed to sevoflurane anesthesia.Heliyon · 2024Article
- SynCAM1 deficiency in the hippocampal parvalbumin interneurons contributes to sevoflurane-induced cognitive impairment in neonatal rats.CNS neuroscience & therapeutics · 2024Article
- Maternal sevoflurane exposure increases the epilepsy susceptibility of adolescent offspring by interrupting interneuron development.BMC medicine · 2023Article
- Lactate Improves Long-term Cognitive Impairment Induced By Repeated Neonatal Sevoflurane Exposures Through SIRT1-mediated Regulation of Adult Hippocampal Neurogenesis and Synaptic Plasticity in Male Mice.Molecular neurobiology · 2023Article
- Sevoflurane induces microRNA-18a to delay rat neurodevelopment via suppression of the RUNX1/Wnt/β-catenin axis.Cell death discovery · 2022Article
- Timely N-Acetyl-Cysteine and Environmental Enrichment Rescue Oxidative Stress-Induced Parvalbumin Interneuron Impairments via MMP9/RAGE Pathway: A Translational Approach for Early Intervention in Psychosis.Schizophrenia bulletin · 2021Article
- Gut microbiota mediates cognitive impairment in young mice after multiple neonatal exposures to sevoflurane.Aging · 2021Article
- [Effect of Long-time Postnatal Exposure to Sevoflurane on Causing Attention-deficit/Hyperactivity Disorder in Rats].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021Article
- Effects of Sevoflurane Exposure During Late Pregnancy on Brain Development and Beneficial Effects of Enriched Environment on Offspring Cognition.Cellular and molecular neurobiology · 2020Article
- Involvement of homodomain interacting protein kinase 2-c-Jun N-terminal kinase/c-Jun cascade in the long-term synaptic toxicity and cognition impairment induced by neonatal Sevoflurane exposure.Journal of neurochemistry · 2020Article
- Disruption of Striatal-Enriched Protein Tyrosine Phosphatase Signaling Might Contribute to Memory Impairment in a Mouse Model of Sepsis-Associated Encephalopathy.Neurochemical research · 2019Article
- Article
- Systemic Inflammation Impairs Mood Function by Disrupting the Resting-State Functional Network in a Rat Animal Model Induced by Lipopolysaccharide Challenge.Mediators of inflammation · 2019Article
- Exercising New Neurons to Vanquish Alzheimer Disease.Brain plasticity (Amsterdam, Netherlands) · 2018Review
- Article
- Effect of repeated neonatal sevoflurane exposure on the learning, memory and synaptic plasticity at juvenile and adult age.American journal of translational research · 2017Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parvalbumin (PV) interneurons are critically involved in the cognitive processes. Based on prior investigations that environmental enrichment reverses impaired cognition after anesthetic exposure, we proposed that environmental enrichment protects PV interneurons and thereby improves sevoflurane-induced cognitive impairments. Six-day-old C57BL/6 male mice were exposed to 3 % sevoflurane or 30 % oxygen/air 2 h daily for 3 days from postnatal day 6 (P6) to P8. The mice were randomly allocated to an enriched environment for 2 h daily between P8 and P90 or a standard environment. Western blotting and immunofluorescence were used for determining PV expression in the prefrontal cortex and hippocampus. In another set of experiments, cognitive tests were assessed by the open field test (P41), Morris water maze test (P54-60), and fear conditioning tests (P42-43 and P89-90). Exposure of neonatal mice to sevoflurane resulted in a reduced freezing response in the contextual test at P43 but not P90. The PV expression in these mice was decreased at P9, P14, P28, and P42, but not at ≥P60. No colocalization of caspase-3 and 5-bromo-2-deoxyuridine or caspase-3 and PV was observed, suggesting that caspase-independent pathways may be involved in the mediation of sevoflurane-induced down-regulation of PV. The sevoflurane-exposed mice that were placed in an enriched environment exhibited normal behavior and had PV interneurons that did not differ from those in the control mice at P42-43. Neonatal sevoflurane exposure induces a reduced freezing response in the contextual test at P43 and developmental delays in PV interneurons in the prefrontal cortex and hippocampus. Placement of the sevoflurane-exposed mice in an enriched environment can prevent these abnormalities.
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