Abstract <p>The developing brain is vulnerable to hypoxic exposure, andtherefore, disruption of fetal oxygen supply leads to impaired formationof brain regions and their functioning in subsequent ontogenesis.The search for neuroprotective drugs that protect offspring fromthe consequences of prenatal hypoxia is an urgent problem. Thisstudy was aimed to evaluate the possibility of correcting negativeeffects of prenatal hypoxia in rats by administering melatonin to pregnantfemales. After a single hypoxic exposure on day 14 of pregnancy(E14), some of the females received melatonin (10 mg/kg) for 5 days(E16–E20). Following prenatal hypoxia, in early postnatal ontogenesis,the offspring exhibited an increased level of stress-induced vocalization,a delay in the maturation of hippocampal nervous tissue, as wellas signs of neuronal pathology and capillary microthrombosis. Melatoninadministration to pregnant females normalized the level of stress-inducedvocalization in the offspring. Ultrastructural analysis of the hippocampusin the offspring of melatonin-treated females showed no signs ofdelayed maturation of nervous tissue, although some pathological alterationsin neurons and blood vessels persisted. The obtained results demonstratea partial correction of the effects of prenatal hypoxia on hippocampal developmentand emotional behavior in rats and are consistent with modern conceptsof the neuroprotective role of melatonin in antenatal and earlypostnatal ontogenesis, thus corroborating the prospects for itsuse in clinical practice for the prevention and mitigation of theconsequences of prenatal hypoxia.</p>