Prenatal hypoxia is a common pathological condition that can adversely influence neuronal development. Oxygen deficiency during critical periods of neurodevelopment interferes with key developmental pathways in the brain and has been associated with persistent neurological deficits. Under hypoxic conditions, disturbances in Ca²⁺ homeostasis, dysregulated excitatory signaling, and mitochondrial dysfunction collectively contribute to brain pathology. Calcium-transporting ATPases play a central role in controlling intracellular Ca²⁺ levels and supporting neuronal function. This study aimed to evaluate the effects of prenatal hypoxia induced during the organogenesis stage on Ca²⁺-ATPase activity in the mitochondrial fraction of selected brain regions of rat pups during postnatal ontogeny. The data showed the most pronounced decrease in Ca²⁺-ATPase activity in 17-day-old offspring exposed to prenatal hypoxia, particularly in the hippocampus, hypothalamus, and the visual, orbital, and limbic cortices. In 30- and 90-day-old animals, reduced enzyme activity was still observed in the hippocampus, as well as in the orbital and limbic cortices. In other analyzed brain areas, Ca²⁺-ATPase activity tended to return toward control levels. Thus, prenatal hypoxia was accompanied by a downregulation of Ca²⁺-ATPase activity, which may lead to an increase in intracellular Ca²⁺ and reflect prolonged alterations in the brain of the offspring.
L.B. Gadirova (Wed,) studied this question.