ArticleBio-protocol2022
A Simplified Paradigm of Late Gestation Transient Prenatal Hypoxia to Investigate Functional and Structural Outcomes from a Developmental Hypoxic Insult.
Article in Bio-protocol, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 0 citations in OpenAlex.
- Acute Seizure Susceptibility and Chronic Vascular Malformation in a Developmental Mouse Model of Sturge-Weber Syndrome.International journal of molecular sciences · 2026Article
- Branched Chain Amino Acid Metabolism in Developmental Brain Injury: Putative Mechanisms and Therapeutic Potential.Developmental neuroscience · 2026Review
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2 authors at 1 institution in 1 country.
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Abstract
Late-gestation transient intrauterine hypoxia is a common cause of birth injury. It can lead to long-term neurodevelopmental disabilities even in the absence of gross anatomic injury. Currently, postnatal models of hypoxia-ischemia are most commonly used to study the effect of oxygen deprivation in the fetal brain. These models, however, are unable to take into account placental factors that influence the response to hypoxia, exhibit levels of cell death not seen in many human patients, and are unable to model preterm hypoxia. To address this gap in research, we have developed a protocol to induce transient hypoxia in fetal mice. A pregnant dam at gestational day 17.5 is placed into a hypoxia chamber. Over 30 min, the inspired oxygen is titrated from 21% (ambient air) to 5%. The dam remains in the chamber for up to 8 h, after which fetal brains can be collected or pups delivered for postnatal studies. This protocol recapitulates phenotypes seen in human patients exposed to transient in utero hypoxia and is readily reproducible by researchers. Graphical abstract.
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