ArticleBritish journal of anaesthesia2018
Inhibition of RhoA reduces propofol-mediated growth cone collapse, axonal transport impairment, loss of synaptic connectivity, and behavioural deficits.
Article in British journal of anaesthesia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- High-Dose Propofol Induces Cytotoxicity by Elevating Intracellular CaDrug design, development and therapy · 2026Article
- RHO GTPase by L1 GABAergic neurons in frontal cortex and L6 glutamatergic neurons in prefrontal cortex differentiates states of unconsciousness.Scientific reports · 2025Article
- Disruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of microRNAs in cognitive decline related to COVID‑19 (Review).Experimental and therapeutic medicine · 2024Review
- Determination of the embryotoxic effects of propofol injected into eggs on the cerebellum and spinal cord using histologic methods: an animal study.Turkish journal of medical sciences · 2024Article
- Prenatal PMParticle and fibre toxicology · 2023Article
- Tau protein plays a role in the mechanism of cognitive disorders induced by anesthetic drugs.Frontiers in neuroscience · 2023Review
- Non-Coding RNAs in the Regulation of Hippocampal Neurogenesis and Potential Treatment Targets for Related Disorders.Biomolecules · 2022Review
- TTC3-Mediated Protein Quality Control, A Potential Mechanism for Cognitive Impairment.Cellular and molecular neurobiology · 2022Review
- lncRNA BDNF-AS Attenuates Propofol-Induced Apoptosis in HT22 Cells by Modulating the BDNF/TrkB Pathway.Molecular neurobiology · 2022Article
- Review
- Subpial delivery of adeno-associated virus 9-synapsin-caveolin-1 (Theranostics · 2022Article
- Cognitive dysfunction associated with COVID-19: Prognostic role of circulating biomarkers and microRNAs.Frontiers in aging neuroscience · 2022Review
- Propofol induces the apoptosis of neural stem cells via microRNA-9-5p / chemokine CXC receptor 4 signaling pathway.Bioengineered · 2022Article
- MicroRNA-31-3p/RhoA signaling in the dorsal hippocampus modulates methamphetamine-induced conditioned place preference in mice.Psychopharmacology · 2021Article
- Synapsin-caveolin-1 gene therapy preserves neuronal and synaptic morphology and prevents neurodegeneration in a mouse model of AD.Molecular therapy. Methods & clinical development · 2021Article
- HCell death discovery · 2021Article
- RTA-408 protects against propofol-induced cognitive impairment in neonatal mice via the activation of Nrf2 and the inhibition of NF-κB p65 nuclear translocation.Brain and behavior · 2021Article
- Maternal sevoflurane exposure affects differentiation of hippocampal neural stem cells by regulating miR-410-3p and ATN1.Stem cell research & therapy · 2020Article
- General Anesthetic-Induced Neurotoxicity in the Immature Brain: Reevaluating the Confounding Factors in the Preclinical Studies.BioMed research international · 2020Review
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Authors and funding
18 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundExposure of the developing brain to propofol results in cognitive deficits. Recent data suggest that inhibition of neuronal apoptosis does not prevent cognitive defects, suggesting mechanisms other than neuronal apoptosis play a role in anaesthetic neurotoxicity. Proper neuronal growth during development is dependent upon growth cone morphology and axonal transport. Propofol modulates actin dynamics in developing neurones, causes RhoA-dependent depolymerisation of actin, and reduces dendritic spines and synapses. We hypothesised that RhoA inhibition prevents synaptic loss and subsequent cognitive deficits. The present study tested whether RhoA inhibition with the botulinum toxin C3 (TAT-C3) prevents propofol-induced synapse and neurite loss, and preserves cognitive function.
methodsRhoA activation, growth cone morphology, and axonal transport were measured in neonatal rat neurones (5-7 days in vitro) exposed to propofol. Synapse counts (electron microscopy), dendritic arborisation (Golgi-Cox), and network connectivity were measured in mice (age 28 days) previously exposed to propofol at postnatal day 5-7. Memory was assessed in adult mice (age 3 months) previously exposed to propofol at postnatal day 5-7.
resultsPropofol increased RhoA activation, collapsed growth cones, and impaired retrograde axonal transport of quantum dot-labelled brain-derived neurotrophic factor, all of which were prevented with TAT-C3. Adult mice previously treated with propofol had decreased numbers of total hippocampal synapses and presynaptic vesicles, reduced hippocampal dendritic arborisation, and infrapyramidal mossy fibres. These mice also exhibited decreased hippocampal-dependent contextual fear memory recall. All anatomical and behavioural changes were prevented with TAT-C3 pre-treatment.
conclusionInhibition of RhoA prevents propofol-mediated hippocampal neurotoxicity and associated cognitive deficits.
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