Prenatal Hypoxia Leads to Impaired Formation of Nervous Tissue in the Entorhinal Area of the Cerebral Cortex in Rats

Prenatal hypoxia impairs brain formation, leading to the development of cognitive deficit in the postnatal period. The probable causes of this deficit may be linked with derangement of the functioning of the dorsal hippocampus and areas of the neocortex involved in its afferentation, particularly th...

Full description

Saved in:
Bibliographic Details
Published in:Neuroscience and behavioral physiology 2021-06, Vol.51 (5), p.681-686
Main Authors: Vasilev, D. S., Tumanova, N. L., Kalinina, D. S.
Format: Article
Language:English
Subjects:
Behavioral Sciences
Biomedical and Life Sciences
Biomedicine
Cell death
Cerebral cortex
Cognitive ability
Cortex (entorhinal)
Electron microscopy
Embryogenesis
Hippocampus
Hypoxia
Interneurons
Juveniles
Lysis
Neocortex
Neurobiology
Neuroblasts
Neurogenesis
Neurons
Neurosciences
Ontogeny
Pregnancy
Pyramidal cells
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Prenatal hypoxia impairs brain formation, leading to the development of cognitive deficit in the postnatal period. The probable causes of this deficit may be linked with derangement of the functioning of the dorsal hippocampus and areas of the neocortex involved in its afferentation, particularly the entorhinal cortex, whose projection neurons innervate field CA1. The aim of the present work was to assess the effects of prenatal hypoxia on formation of nervous tissues in the entorhinal cortex during early ontogeny in rats subjected to prenatal hypoxia on days 14 or 18 of embryogenesis. In vivo labeling of neuroblasts formed in embryos at the moment of exposure to hypoxia with 3’-ethinyl-5-deoxyuridine showed that depending on the time of exposure, hypoxia impaired the formation and migration of neuroblasts to the lower (hypoxia on day 14 of pregnancy) or upper (hypoxia on day 18) layers of the entorhinal cortex. Hypoxia on E14 but not E18 led to a reduction in the number of neurons in the entorhinal cortex in rat pups in the first month of postnatal ontogeny. This reduction is evidence of neuron death. Impairment to the process of neurogenesis affected the formation of projection pyramidal neurons but had no effect on the population of inhibitory interneurons. Electron microscopy revealed pathological changes to neurons in the entorhinal cortex of rat pups on postnatal day 20 (cytoplasmic organelle lysis or hyperchromatosis). Hypoxia on day 18 of pregnancy produced no changes in cell composition or pyramidal neuron death in the postnatal period in the offspring. Prenatal hypoxia on day E14 evidently leads to impairment to the radial migration of neuroblasts in the entorhinal cortex and increases elimination of projection neurons in early postnatal ontogeny. Projection neuron death in the entorhinal cortex can lead to impairment to afferentation of hippocampal neurons. The selective action of prenatal hypoxia on the excitatory neuron population of the entorhinal cortex of the rat cerebral cortex may lead to disturbance of the balance between excitatory and inhibitory processes during subsequent development.
ISSN:0097-0549
1573-899X
DOI:10.1007/s11055-021-01121-2