Sevoflurane-induced neurotoxicity (SIN) model in rats

This comprehensive animal model study investigated the neuromorphopathological underpinnings of prolonged sevoflurane anesthesia-induced neurotoxicity. The researchers established a SIN model using prolonged sevoflurane exposure and examined its effects on cognitive function, anxiety-like behaviors, neuroinflammation, and synaptic integrity. The study employed multiple behavioral assays (Morris water maze, elevated plus maze, open field test) to assess cognitive dysfunction and anxiety. Molecular analyses included transcriptomic profiling via RNA sequencing, electrophysiology to measure neuronal excitability, and various histological techniques. The researchers discovered that prolonged anesthesia activated the NF-κB inflammatory pathway, triggered neuroinflammation, and led to complement-mediated microglial synaptic elimination. Key findings included increased microglial activation and phagocytosis, upregulation of complement components C1qa and C3, synaptic loss in the hippocampus, and reduced dendritic spines.

This comprehensive animal model study investigated the neuromorphopathological underpinnings of prolonged sevoflurane anesthesia-induced neurotoxicity. The researchers established a SIN model using prolonged sevoflurane exposure and examined its effects on cognitive function, anxiety-like behaviors, neuroinflammation, and synaptic integrity. The study employed multiple behavioral assays (Morris water maze, elevated plus maze, open field test) to assess cognitive dysfunction and anxiety. Molecular analyses included transcriptomic profiling via RNA sequencing, electrophysiology to measure neuronal excitability, and various histological techniques. The researchers discovered that prolonged anesthesia activated the NF-κB inflammatory pathway, triggered neuroinflammation, and led to complement-mediated microglial synaptic elimination. Key findings included increased microglial activation and phagocytosis, upregulation of complement components C1qa and C3, synaptic loss in the hippocampus, and reduced dendritic spines. Intervention studies involving microglial depletion, neuroinflammation inhibition, and C1q neutralization demonstrated rescue of synaptic loss and behavioral deficits, establishing the therapeutic relevance of targeting this pathway.