ArticleCNS neuroscience & therapeutics2024
SynCAM1 deficiency in the hippocampal parvalbumin interneurons contributes to sevoflurane-induced cognitive impairment in neonatal rats.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 11 citations in OpenAlex.
- Single-Nucleus Transcriptomic Landscape of Neonatal Mice Hippocampus During Sevoflurane-Induced Neurotoxicity.Neurochemical research · 2025Article
- Rutin ameliorates sevoflurane-induced neurotoxicity by inhibiting microglial synaptic phagocytosis through the complement pathway.Scientific reports · 2025Article
- Photo-Biomodulation of the Hippocampus Using Near-Infrared Laser to Enhance Cognitive Function in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Environmental enrichment alleviates neuropathic pain-associated anxiety by enhancing the function of parvalbumin interneurons in the anterior cingulate cortex.Scientific reports · 2025Article
- Decoding pain's neural rhythm: Gamma oscillation mechanisms, therapeutic modulation, and translational challenges in pain management.Frontiers in neuroscience · 2025Review
- SynCAM1 deficiency in the hippocampal parvalbumin interneurons contributes to sevoflurane-induced cognitive impairment in neonatal rats.CNS neuroscience & therapeutics · 2024Article
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8 authors at 2 institutions in 1 country.
Funding
Abstract
aimsSevoflurane is widely used for general anesthesia in children. Previous studies reported that multiple neonatal exposures to sevoflurane can induce long-term cognitive impairment in adolescent rats, but the underlying mechanisms were not defined.
methodsPostnatal day 6 (P6) to P8 rat pups were exposed to 30% oxygen with or without 3% sevoflurane balanced with air. The Y maze test (YMT) and Morris water maze (MWM) tests were performed in some cohorts from age P35 to assess cognitive functions, and their brain samples were harvested at age P14, 21, 28, 35, and 42 for measurements of various molecular entities and in vivo electrophysiology experiments at age P35.
resultsSevoflurane exposure resulted in cognitive impairment that was associated with decreased synCAM1 expression in parvalbumin (PV) interneurons, a reduction of PV phenotype, disturbed gamma oscillations, and dendritic spine loss in the hippocampal CA3 region. Enriched environment (EE) increased synCAM1 expression in the PV interneurons and attenuated sevoflurane-induced cognitive impairment. The synCAM1 overexpression by the adeno-associated virus vector in the hippocampal CA3 region restored sevoflurane-induced cognitive impairment, PV phenotype loss, gamma oscillations decrease, and dendritic spine loss.
conclusionOur data suggested that neonatal sevoflurane exposure results in cognitive impairment through decreased synCAM1 expression in PV interneurons in the hippocampus.
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