However, hypoxia did not affect gestational age at birth, litter size at birth, or pup survival. Hypoxia exposure predisposed animals to decreased weight at postnatal day 2, which normalized by day 8. Late gestation transient prenatal hypoxia increased hypoxia-inducible factor 1 alpha protein levels (a marker of hypoxic exposure) in the fetal brain. Therefore, here we characterized the effect of late gestation (embryonic day 17.5) transient prenatal hypoxia (5% inspired oxygen) on long-term anatomical and neurodevelopmental outcomes in mice. However, these large animal studies are resource-intensive and not readily amenable to mechanistic molecular studies. Furthermore, large animal models suggest that transient prenatal hypoxia without ischemia is sufficient to lead to significant functional impairment to the developing brain. The published rodent models of prenatal hypoxia employ multiple days of hypoxic exposure or complicated surgical procedures, making these models challenging to perform consistently in mice. Prenatal models of hypoxia in mice may allow us to address some of these limitations to expand our understanding of developmental brain injury. Lastly, they do not model preterm hypoxic injury. Second, they primarily recapitulate severe injury because they provoke substantial cell death, which is not seen in children with mild hypoxic injury. First, they do not test the impact of placental pathologies on outcomes from hypoxia. Postnatal models, however, have some limitations. Postnatal hypoxia-ischemia rodent models are commonly used to understand the effects of ischemia and transient hypoxia on the developing brain. Intrauterine hypoxia is a common cause of brain injury in children resulting in a broad spectrum of long-term neurodevelopmental sequela, including life-long disabilities that can occur even in the absence of severe neuroanatomic damage.
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