ArticleBirth defects research. Part B, Developmental and reproductive toxicology2014
Ketamine affects the neurogenesis of rat fetal neural stem progenitor cells via the PI3K/Akt-p27 signaling pathway.
Article in Birth defects research. Part B, Developmental and reproductive toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Consensus Statement on Pain Management for Pregnant Patients with Opioid-Use Disorder from the Society for Obstetric Anesthesia and Perinatology, Society for Maternal-Fetal Medicine, and American Society of Regional Anesthesia and Pain Medicine.Anesthesia and analgesia · 2025Guideline
- Calcium Signaling Dysregulation as a Convergent Mechanism in Anesthetic-Induced Developmental Neurotoxicity.Drug design, development and therapy · 2026Review
- Ketamine use disorder: preclinical, clinical, and neuroimaging evidence to support proposed mechanisms of actions.Intelligent medicine · 2022Article
- Review
- Review
- Blockade of the NLRP3/caspase-1 axis attenuates ketamine-induced hippocampus pyroptosis and cognitive impairment in neonatal rats.Journal of neuroinflammation · 2021Article
- Article
- General Anesthetic-Induced Neurotoxicity in the Immature Brain: Reevaluating the Confounding Factors in the Preclinical Studies.BioMed research international · 2020Review
- Effects of Perinatal Exposure to Ketamine on the Developing Brain.Frontiers in neuroscience · 2019Review
- Management of eight labor and delivery patients dependent on buprenorphine (Subutex™): A retrospective chart review.F1000Research · 2018Article
- Ketamine Modulates Zic5 Expression via the Notch Signaling Pathway in Neural Crest Induction.Frontiers in molecular neuroscience · 2018Article
- Article
- Article
- Ketamine exposure during embryogenesis inhibits cellular proliferation in rat fetal cortical neurogenic regions.Acta anaesthesiologica Scandinavica · 2016Article
- Ethosuximide Induces Hippocampal Neurogenesis and Reverses Cognitive Deficits in an Amyloid-β Toxin-induced Alzheimer Rat Model via the Phosphatidylinositol 3-Kinase (PI3K)/Akt/Wnt/β-Catenin Pathway.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Ketamine is widely used as an anesthetic, analgesic, or sedative in pediatric patients. We reported that ketamine alters the normal neurogenesis of rat fetal neural stem progenitor cells (NSPCs) in the developing brain, but the underlying mechanisms remain unknown. The PI3K-PKB/Akt (phosphatidylinositide 3-kinase/protein kinase B) signaling pathway plays many important roles in cell survival, apoptosis, and proliferation. We hypothesized that PI3K-PKB/Akt signaling may be involved in ketamine-altered neurogenesis of cultured NSPCs in vitro. NSPCs were isolated from Sprague-Dawley rat fetuses on gestational day 17. 5-bromo-2'-deoxyuridine (BrdU) incorporation, Ki67 staining, and differentiation tests were utilized to identify primary cultured NSPCs. Immunofluorescent staining was used to detect Akt expression, whereas Western blots measured phosphorylated Akt and p27 expression in NSPCs exposed to different treatments. We report that cultured NSPCs had properties of neurogenesis: proliferation and neural differentiation. PKB/Akt was expressed in cultured rat fetal cortical NSPCs. Ketamine inhibited the phosphorylation of Akt and further enhanced p27 expression in cultured NSPCs. All ketamine-induced PI3K/Akt signaling changes could be recovered by N-methyl-d-aspartate (NMDA) receptor agonist, NMDA. These data suggest that the inhibition of PI3K/Akt-p27 signaling may be involved in ketamine-induced neurotoxicity in the developing brain, whereas excitatory NMDA receptor activation may reverse these effects.
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