ArticleFrontiers in cellular neuroscience2023
Xenon inhalation attenuates neuronal injury and prevents epilepsy in febrile seizure Sprague-Dawley pups.
Article in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- TREM2-mediated microglial phagocytosis of inhibitory synapses contributes to prolonged FS-induced epileptogenesis.Cell death discovery · 2026Article
- Salidroside Attenuates Epilepsy and Cognitive Dysfunction in Rats by Downregulating Complement C3-C3aR Pathway-Mediated Activation of Microglia and Astrocytes.Neurochemical research · 2025Article
- Xenon gas as a potential treatment for opioid use disorder, alcohol use disorder, and related disorders.Medical gas research · 2025Review
- Increased thrombospondin-1 levels contribute to epileptic susceptibility in neonatal hyperthermia without seizures via altered synaptogenesis.Cell death discovery · 2024Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Febrile seizures (FS) usually occur in childhood and may cause irreversible neuronal damage, cognitive functional defects, and an increase in the risk of epilepsy later in life. Anti-epileptic drugs (AEDs), currently used to treat FS in children, can relieve seizures. However, their effects in preventing the risk of developing epilepsy in later life are unsatisfactory. Moreover, AEDs may damage child brain development. Here, we evaluated the efficiency of xenon in treating prolonged FS (PFS) and preventing epilepsy in Sprague-Dawley pups. Methods: Prolonged FS was induced by hyperthermic treatment. After 90 min of PFS, the pups in the xenon treatment group were immediately treated with 70% xenon/21% oxygen/9% nitrogen for 60 min. The levels of glutamate, mitochondrial oxidative stress, mitophagy, and neuronal injury, seizures, learning, and memory functions were measured at specific time points. Results: Neonatal period PFS led to spontaneous seizure, learning and memory dysfunction, accompanied by increased levels of glutamate, mitochondrial oxidative stress, mitophagy, and neuronal injury. Xenon treatment alleviated the changes caused by PFS and reduced the risk of PFS developing into epilepsy later. Conclusion: Our results suggest that xenon inhalation could be a potential therapeutic strategy to attenuate neuronal injury and prevent epilepsy in patients with FS.
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