The developing brain is vulnerable to hypoxic exposure, and therefore, disruption of fetal oxygen supply leads to impaired formation of brain regions and their functioning in subsequent ontogenesis. The search for neuroprotective drugs that protect offspring from the consequences of prenatal hypoxia is an urgent problem. This study was aimed to evaluate the possibility of correcting negative effects of prenatal hypoxia in rats by administering melatonin to pregnant females. 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 well as signs of neuronal pathology and capillary microthrombosis. Melatonin administration to pregnant females normalized the level of stress-induced vocalization in the offspring. Ultrastructural analysis of the hippocampus in the offspring of melatonin-treated females showed no signs of delayed maturation of nervous tissue, although some pathological alterations in neurons and blood vessels persisted. The obtained results demonstrate a partial correction of the effects of prenatal hypoxia on hippocampal development and emotional behavior in rats and are consistent with modern concepts of the neuroprotective role of melatonin in antenatal and early postnatal ontogenesis, thus corroborating the prospects for its use in clinical practice for the prevention and mitigation of the consequences of prenatal hypoxia.
Dubrovskaya et al. (Wed,) studied this question.