The Influence of Chronic Prenatal Hypoxia on the Functional State of Mice and Their Adaptation to Audiogenic Seizures

Prenatal hypoxia remains the leading cause of infant mortality and severe disability in newborns. Disturbances in the development of fetal brain structures and functions due to hypoxic damage are the main trigger for the development of severe neurological disorders and accelerated neurodegeneration processes and can also be the cause of epileptiform activity in the postnatal period. Herein, the role of chronic prenatal hypoxia on the functional state of C3H+C57Bl6 hybrid mice during the first three weeks of postnatal development and the risks of developing epileptiform activity when provoking audiogenic seizures were assessed. Exposure to chronic prenatal hypoxia was found to increase the risk of neonatal mortality and developmental delay in the surviving individuals in the first two weeks of the postnatal period. It was shown that one of the causes of the failure of adaptation might be the disruption of the functional activity of the mitochondrial apparatus of brain cells mediated by the disruption of the first and second respiratory chain complexes. Exposure to chronic prenatal hypoxia has no significant effect on the increased risk of seizure activity in mice during audiogenic stimulation in late postnatal development, does not activate the development of persistent neurological deficit, and does not significantly affect the cognitive functions and learning ability of animals.