Neonatal hypoxic ischemic encephalopathy (HIE) is a leading cause of neurodevelopmental disease secondary to brain injury. Most murine models of HIE produce injury postnatally, after early neonatal milestones have already emerged. We have previously shown that transient prenatal hypoxia leads to long-term neuroanatomical and behavioral deficits. We now hypothesize that mice exposed to in utero hypoxia have short-term deficits, including early deficits in neuronal structure and neonatal behaviors.