Abstract

The issues of brain morphogenesis during the early postnatal period and the effect of perinatal hypoxia thereupon, which can lead to the development of neuropsychic pathology, are among the major medical and social challenges. It is well known that the nucleoli of neocortical neurons synthesize ribosomal subunits and are involved in various morphogenetic processes. When studying the effect of perinatal hypoxia on the developing brain in the model of neonatal encephalopathy, we revealed ultrastructural changes in the nucleoli of neocortical neurons and in the numerical ratio of their types. In control rats, as they develop in the neonatal period, there is an increase in the number of both granular and reticulated nucleolar types, which may be due to ribosomal RNA (rRNA) processing. By the end of the neonatal period, the emergence of granular agglomerates (ribosomal subunits) near the nuclear membrane may be due to nerve cell differentiation and the biogenesis of the rough endoplasmic reticulum. In the present work, we established the fact of changing the numerical ratio of the granular and reticulated nucleolar types in the nuclei of neocortical neurons after perinatal hypoxic exposure of experimental vs. control rats. Our data suggest that the nucleoli in neocortical neurons are the targets for the exposure to perinatal hypoxia, i.e. a link in the pathogenesis of this disease. Post-hypoxic administration of Phenibut (a GABA derivative, nootropic drug) corrected the pathogenetic effect of perinatal hypoxia by restoring the numerical ratio of the nucleolar types in neocortical neurons, which is inherent to control rats. We assume that Phenibut can exert a neuroprotective effect through its ability to affect the nucleolar ultrastructure in neocortical neurons.

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