ArticleNeurobiology of disease2012
The abolishment of anesthesia-induced cognitive impairment by timely protection of mitochondria in the developing rat brain: the importance of free oxygen radicals and mitochondrial integrity.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 152 citations in OpenAlex.
- Effects of Repeated Early-life Anesthesia Exposure on Visual System Development in Mice.Anesthesiology · 2026Article
- Methylene Blue for Prevention of Perioperative Neurocognitive Disorders: Mechanisms and Recent Clinical Evidence.Drug design, development and therapy · 2026Review
- Unraveling the role and mechanism of mitochondria in postoperative cognitive dysfunction: a narrative review.Journal of neuroinflammation · 2024Review
- Cenobamate suppresses seizures without inducing cell death in neonatal rats.Epilepsy & behavior : E&B · 2024Article
- A primordial target: Mitochondria mediate both primary and collateral anesthetic effects of volatile anesthetics.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Hot Spots for the Use of Intranasal Insulin: Cerebral Ischemia, Brain Injury, Diabetes Mellitus, Endocrine Disorders and Postoperative Delirium.International journal of molecular sciences · 2023Review
- Parvalbumin interneuron loss mediates repeated anesthesia-induced memory deficits in mice.The Journal of clinical investigation · 2023Article
- The effects of general anesthetics on mitochondrial structure and function in the developing brain.Frontiers in neurology · 2023Review
- Future directions in ventilator-induced lung injury associated cognitive impairment: a new sight.Frontiers in physiology · 2023Review
- Caspase-3 Inhibition toward Perinatal Protection of the Developing Brain from Environmental Stress.Developmental neuroscience · 2023Review
- Neonatal exposures to sevoflurane in rhesus monkeys alter synaptic ultrastructure in later life.iScience · 2022Article
- Percutaneous Closure of Patent Ductus Arteriosus.Clinics in perinatology · 2022Review
- Do We Have Viable Protective Strategies against Anesthesia-Induced Developmental Neurotoxicity?International journal of molecular sciences · 2022Review
- Protective Effects of Pioglitazone on Cognitive Impairment and the Underlying Mechanisms: A Review of Literature.Drug design, development and therapy · 2022Review
- Tetraethylammonium chloride reduces anaesthetic-induced neurotoxicity in Caenorhabditis elegans and mice.British journal of anaesthesia · 2022Article
- Intranasal insulin rescues repeated anesthesia-induced deficits in synaptic plasticity and memory and prevents apoptosis in neonatal mice via mTORC1.Scientific reports · 2021Article
- Intranasal levosimendan prevents cognitive dysfunction and apoptotic response induced by repeated isoflurane exposure in newborn rats.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Singular and short-term anesthesia exposure in the developing brain induces persistent neuronal changes consistent with chronic neurodegenerative disease.Scientific reports · 2021Article
- A synthetic peptide rescues rat cortical neurons from anesthetic-induced cell death, perturbation of growth and synaptic assembly.Scientific reports · 2021Article
- Inhibition ofOxidative medicine and cellular longevity · 2021Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Early exposure to general anesthesia (GA) causes developmental neuroapoptosis in the mammalian brain and long-term cognitive impairment. Recent evidence suggests that GA also causes functional and morphological impairment of the immature neuronal mitochondria. Injured mitochondria could be a significant source of reactive oxygen species (ROS), which, if not scavenged in timely fashion, may cause excessive lipid peroxidation and damage of cellular membranes. We examined whether early exposure to GA results in ROS upregulation and whether mitochondrial protection and ROS scavenging prevent GA-induced pathomorphological and behavioral impairments. We exposed 7-day-old rats to GA with or without either EUK-134, a synthetic ROS scavenger, or R(+) pramipexole (PPX), a synthetic aminobenzothiazol derivative that restores mitochondrial integrity. We found that GA causes extensive ROS upregulation and lipid peroxidation, as well as mitochondrial injury and neuronal loss in the subiculum. As compared to rats given only GA, those also given PPX or EUK-134 had significantly downregulated lipid peroxidation, preserved mitochondrial integrity, and significantly less neuronal loss. The subiculum is highly intertwined with the hippocampal CA1 region, anterior thalamic nuclei, and both entorhinal and cingulate cortices; hence, it is important in cognitive development. We found that PPX or EUK-134 co-treatment completely prevented GA-induced cognitive impairment. Because mitochondria are vulnerable to GA-induced developmental neurotoxicity, they could be an important therapeutic target for adjuvant therapy aimed at improving the safety of commonly used GAs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.