ArticleCNS neuroscience & therapeutics2025
Repeated Exposure to Sevoflurane in Neonatal Mice Induces Cognitive and Synaptic Impairments in a TTLL6-Mediated Tubulin Polyglutamylation Manner.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Dexmedetomidine Mitigates Sevoflurane-Induced Neurodevelopmental Effects in Paediatric Anaesthesia: A Meta-Analysis and Preclinical Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Pooled it
- Environmental enrichment mitigates sevoflurane-induced neurodevelopmental injury via cGAS-STING-dependent microglial modulation.Cell & bioscience · 2026Article
- Targeting Ferroptosis Pathways for Synaptic Protection in Sevoflurane-Induced Cognitive Impairment: A Nanomedicine Approach.CNS neuroscience & therapeutics · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
aimsRepeated sevoflurane exposure during the neonatal stage may induce Tau phosphorylation, dendritic spine loss, and neurocognitive impairment in the developing brain. Tubulin tyrosine ligase like-6 (TTLL6), which aggregates in dendrites due to Tau missorting, regulates microtubule stability via α-tubulin polyglutamylation. Meanwhile, Spastin modulates dendritic spine formation by severing microtubules. We hypothesize that repeated sevoflurane treatment impairs dendritic spine remodeling in neonatal mice by enhancing TTLL6-mediated tubulin polyglutamylation and increasing Spastin expression, leading to cognitive dysfunction in their pre-adolescent stage.
methodsSix-day-old wild type (WT), TTLL6 brain conditional knockout (TTLL6
resultsRepeated sevoflurane exposure during brain development in neonatal mice could reduce dendritic spine density, synapse number, PSD95, and ATP levels, while increasing pTau, polyglutamylated tubulin, Tau-TTLL6 missorting from axons to the somatodendritic compartment, and Spastin levels, leading to cognitive impairment later in their pre-adolescent stage (P30). However, these changes were ameliorated in the TTLL6
conclusionsRepeated neonatal sevoflurane exposure results in synaptic impairment through TTLL6-mediated tubulin polyglutamylation and increased Spastin expression, causing pre-adolescent cognitive dysfunction in mice. This process is initiated by Tau phosphorylation and missorting from axons to somatodendritic compartments.
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