ArticleNeurotoxicity research2016
Reactive Oxygen Species-mediated Loss of Phenotype of Parvalbumin Interneurons Contributes to Long-term Cognitive Impairments After Repeated Neonatal Ketamine Exposures.
Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Baicalein alleviates long-term cognitive impairments induced by repeated neonatal sevoflurane exposure via inhibition of cortical microglial TLR4/NF-kB signaling.Brain, behavior, & immunity - health · 2025Article
- Timed fetal inflammation and postnatal hypoxia cause cortical white matter injury, interneuron imbalances, and behavioral deficits in a double-hit rat model of encephalopathy of prematurity.Brain, behavior, & immunity - health · 2024Article
- Endoplasmic Reticulum Stress-Activated Neuronal and Microglial Autophagy Contributes to Postoperative Cognitive Dysfunction in Neonatal rats.Neurochemical research · 2023Article
- Neonatal Anesthesia and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- (R,S)-ketamine and (2R,6R)-hydroxynorketamine differentially affect memory as a function of dosing frequency.Translational psychiatry · 2021Article
- Modulating neuroinflammation and oxidative stress to prevent epilepsy and improve outcomes after traumatic brain injury.Neuropharmacology · 2020Review
- Iron overload contributes to general anaesthesia-induced neurotoxicity and cognitive deficits.Journal of neuroinflammation · 2020Article
- Ketamine exerts neurotoxic effects on the offspring of pregnant rats via the Wnt/β-catenin pathway.Environmental science and pollution research international · 2020Article
- Early Celastrol Administration Prevents Ketamine-Induced Psychotic-Like Behavioral Dysfunctions, Oxidative Stress and IL-10 Reduction in The Cerebellum of Adult Mice.Molecules (Basel, Switzerland) · 2019Article
- RvD1binding with FPR2 attenuates inflammation via Rac1/NOX2 pathway after neonatal hypoxic-ischemic injury in rats.Experimental neurology · 2019Article
- Inhibition of NADPH oxidase by apocynin prevents learning and memory deficits in a mouse Parkinson's disease model.Redox biology · 2019Article
- Ketamine-Treatment During Late Adolescence Impairs Inhibitory Synaptic Transmission in the Prefrontal Cortex and Working Memory in Adult Rats.Frontiers in cellular neuroscience · 2019Article
- Effects of Perinatal Exposure to Ketamine on the Developing Brain.Frontiers in neuroscience · 2019Review
- The use of antioxidant compounds in the treatment of first psychotic episode: Highlights from preclinical studies.CNS neuroscience & therapeutics · 2018Review
- Early Intervention and a Direction of Novel Therapeutics for the Improvement of Functional Outcomes in Schizophrenia: A Selective Review.Frontiers in psychiatry · 2018Review
- A Mini-Review of the NADPH oxidases in Vascular Dementia: Correlation with NOXs and Risk Factors for VaD.International journal of molecular sciences · 2017Review
- Ketamine administered pregnant rats impair learning and memory in offspring via the CREB pathway.Oncotarget · 2017Article
- p47Phox/CDK5/DRP1-Mediated Mitochondrial Fission Evokes PV Cell Degeneration in the Rat Dentate Gyrus Following Status Epilepticus.Frontiers in cellular neuroscience · 2017Article
- Elamipretide (SS-31) Ameliorates Isoflurane-Induced Long-Term Impairments of Mitochondrial Morphogenesis and Cognition in Developing Rats.Frontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ketamine, a common anesthetic used for pediatric patients, has been shown to induce neurotoxicity and alter adolescent behaviors in rats when administered during neonatal period. However, the mechanisms underlying this kind of neurotoxicity remain largely to be determined. Herein, we studied whether the reactive oxygen species (ROS) due to the increased NOX2 mediates loss of phenotype of PV interneurons and thus contributes to long-term cognitive impairments after repeated ketamine exposures. Sprague-Dawley male rat pups received a daily administration of ketamine intraperitoneally (75 mg/kg) from postnatal day 6 (P6) to P8 for three consecutive days. For the interventional study, pups were treated with a NADPH oxidase inhibitor, apocynin (Apo). Learning and memory abilities were tested by the open field, fear conditioning, and Morris water maze on P40, P42-44, and P50-56, respectively. For histological and biochemical assays, a separate cohort of rats was killed on P9 or P60, and the brain tissues were harvested. Our results showed the upregulation of 8-OHdG and gp91/NOX2 and downregulation of PV and glutamic acid decarboxylase 67 (GAD67) after repeated ketamine exposures, which co-occurred with the long-term cognitive impairments as evidenced by the decreased freezing time to context. However, Apo treatment attenuated these abnormalities. Our results suggest that oxidative damage, probably due to the increased NOX2, mediates loss of phenotype of PV interneurons and thus contributes to long-term cognitive impairments after repeated ketamine exposures. Moreover, the inhibition of NADPH oxidase may protect against cognitive dysfunction.
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