Пренатальная гипоксия приводит к нарушению формирования нервной ткани энторинальной области коры мозга крыс

Abstract

Prenatal hypoxia disturbs the formation of the brain, which leads to the development of cognitive deficit. The probable causes of this deficiency may be associated with impaired functioning of the dorsal hippocampus as well as the cortical areas involved in its afferentation, in particular the entorhinal cortex, projection neurons of which innervate the CA1 field. This study was performed to analyze the effect of prenatal hypoxia on the population of pyramidal neurons of the entorhinal cortex in early rat ontogenesis. Female Wistar rats were subjected to hypoxia on 14 or 18th days of pregnancy. The neuroblasts formed in embryos at the time of hypoxia were labeled by 3’-ethynyl-5-deoxyurenedine. The number of labeled cells and their and location in the entorhinal cortex was analyzed in 5-day old rat pups. It was shown that hypoxia disturbed the formation and migration of neuroblasts into the superficial (hypoxia on E18) or lower (hypoxia on E14) layers of the entorhinal cortex, leading to death of pyramidal neurons in the first month of postnatal ontogenesis, but did not affect the formation of inhibitory interneurons. Electron microscopy also revealed degenerative changes in the neurons of the entorhinal cortex in rat pups subjected to hypoxia on E14 (lysis of organelles or hyperchromatosis). It can be suggested that prenatal hypoxia lead to impaired radial migration of neuroblasts in the entorhinal cortex, increased elimination of projection neurons in early postnatal ontogenesis, causing impaired afferentation of hypocampal neurons. The selective effect of prenatal hypoxia on the population of exciting neurons of the cerebral cortex can lead to some disturbance in the balance of the processes of excitation and inhibition in the further development.