ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Neonatal hyperoxia exposure disrupts axon-oligodendrocyte integrity in the subcortical white matter.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- Neonatal hyperoxia exposure causes cerebellar lesions and behavioral abnormalities in rats.Scientific reports · 2026Article
- Prolonged Hyperoxia Exposure is an Independent Predictor for Moderate to Severe Neurodevelopmental Impairment in Extremely Premature Neonates.Research square · 2025Article
- Prenatal inflammation exacerbates hyperoxia-induced neonatal brain injury.Journal of neuroinflammation · 2025Article
- Review
- 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
- Review
- Review
- Cerebral Myelination in a Bronchopulmonary Dysplasia Murine Model.Children (Basel, Switzerland) · 2023Article
- Association between bronchopulmonary dysplasia and death or neurodevelopmental impairment at 3 years in preterm infants without severe brain injury.Frontiers in neurology · 2023Article
- Oxidative Stress-Induced Damage to the Developing Hippocampus Is Mediated by GSK3β.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Fetal Zone Steroids Show Discrete Effects on Hyperoxia-Induced Attenuation of Migration in Cultured Oligodendrocyte Progenitor Cells.Oxidative medicine and cellular longevity · 2022Article
- Perinatal Hyperoxia and Developmental Consequences on the Lung-Brain Axis.Oxidative medicine and cellular longevity · 2022Review
- Impaired Cognitive Performance in Mice Exposed to Prolonged Hyperoxia.Advances in experimental medicine and biology · 2022Article
- Persistent myelin abnormalities in a third trimester-equivalent mouse model of fetal alcohol spectrum disorder.Alcoholism, clinical and experimental research · 2022Article
- Cerebellar development after preterm birth.Frontiers in cell and developmental biology · 2022Review
- Nodes of Ranvier during development and repair in the CNS.Nature reviews. Neurology · 2020Review
- Missing in Action: Dysfunctional RNA Metabolism in Oligodendroglial Cells as a Contributor to Neurodegenerative Diseases?Neurochemical research · 2020Review
- Repetitive Erythropoietin Treatment Improves Long-Term Neurocognitive Outcome by Attenuating Hyperoxia-Induced Hypomyelination in the Developing Brain.Frontiers in neurology · 2020Article
- Adverse neuropsychiatric development following perinatal brain injury: from a preclinical perspective.Pediatric research · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The pathological mechanisms underlying neurological deficits observed in individuals born prematurely are not completely understood. A common form of injury in the preterm population is periventricular white matter injury (PWMI), a pathology associated with impaired brain development. To mitigate or eliminate PWMI, there is an urgent need to understand the pathological mechanism(s) involved on a neurobiological, structural, and functional level. Recent clinical data suggest that a percentage of premature infants experience relative hyperoxia. Using a hyperoxic model of premature brain injury, we have previously demonstrated that neonatal hyperoxia exposure in the mouse disrupts development of the white matter (WM) by delaying the maturation of the oligodendroglial lineage. In the present study, we address the question of how hyperoxia-induced alterations in WM development affect overall WM integrity and axonal function. We show that neonatal hyperoxia causes ultrastructural changes, including: myelination abnormalities (i.e., reduced myelin thickness and abnormal extramyelin loops) and axonopathy (i.e., altered neurofilament phosphorylation, paranodal defects, and changes in node of Ranvier number and structure). This disruption of axon-oligodendrocyte integrity results in the lasting impairment of conduction properties in the adult WM. Understanding the pathology of premature PWMI injury will allow for the development of interventional strategies to preserve WM integrity and function.
Indexed as
Identifiers
What OpenQuestion holds
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.