ArticlePloS one2012
Neurodevelopmental consequences of sub-clinical carbon monoxide exposure in newborn mice.
Article in PloS one, 2012. 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.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Medical Gas Therapy for Tissue, Organ, and CNS Protection: A Systematic Review of Effects, Mechanisms, and Challenges.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Pooled it
- Revisiting the sigma-1 receptor as a biological target to treat affective and cognitive disorders.Neuroscience and biobehavioral reviews · 2022Review
- A mechanistic view on the neurotoxic effects of air pollution on central nervous system: risk for autism and neurodegenerative diseases.Environmental science and pollution research international · 2021Review
- Inhaled Gases for Neuroprotection of Neonates: A Review.Frontiers in pediatrics · 2019Review
- Critical Role of Nrf2 in Experimental Ischemic Stroke.Frontiers in pharmacology · 2019Review
- A Pilot Study of Inhaled CO Therapy in Neonatal Hypoxia-Ischemia: Carboxyhemoglobin Concentrations and Brain Volumes.Frontiers in pediatrics · 2018Article
- Carbon monoxide incompletely prevents isoflurane-induced defects in murine neurodevelopment.Neurotoxicology and teratology · 2017Article
- Nicotinic cholinergic system alterations and nitrous oxide exposure in a mouse model: a hypothesis for the pathobiology of autism spectrum disorder.Psychopharmacology · 2017Article
- The BTBR mouse model, cholinergic transmission, and environmental exposure to nitrous oxide.Psychopharmacology · 2017Article
- Anesthesia-Related Carbon Monoxide Exposure: Toxicity and Potential Therapy.Anesthesia and analgesia · 2016Review
- Good gas, bad gas: isoflurane, carbon monoxide, and which is which?Anesthesia and analgesia · 2014Article
- Subclinical carbon monoxide limits apoptosis in the developing brain after isoflurane exposure.Anesthesia and analgesia · 2014Article
- Programmed cell death is impaired in the developing brain of FMR1 mutants.Developmental neuroscience · 2013Article
- Carbon monoxide and anesthesia-induced neurotoxicity.Neurotoxicology and teratologyReview
- Carbon monoxide pollution and neurodevelopment: A public health concern.Neurotoxicology and teratologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Carbon monoxide (CO) exposure at high concentrations results in overt neurotoxicity. Exposure to low CO concentrations occurs commonly yet is usually sub-clinical. Infants are uniquely vulnerable to a variety of toxins, however, the effects of postnatal sub-clinical CO exposure on the developing brain are unknown. Apoptosis occurs normally within the brain during development and is critical for synaptogenesis. Here we demonstrate that brief, postnatal sub-clinical CO exposure inhibits developmental neuroapoptosis resulting in impaired learning, memory, and social behavior. Three hour exposure to 5 ppm or 100 ppm CO impaired cytochrome c release, caspase-3 activation, and apoptosis in neocortex and hippocampus of 10 day old CD-1 mice. CO increased NeuN protein, neuronal numbers, and resulted in megalencephaly. CO-exposed mice demonstrated impaired memory and learning and reduced socialization following exposure. Thus, CO-mediated inhibition of neuroapoptosis might represent an important etiology of acquired neurocognitive impairment and behavioral disorders in children.
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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.