Impaired Cortical Cytoarchitecture and Reduced Excitability of Deep-Layer Neurons in the Offspring of Diabetic Rats

Maternal diabetes has been related to low verbal task scores, impaired fine and gross motor skills, and poor performance in graphic and visuospatial tasks during childhood. The primary motor cortex is important for controlling motor functions, and embryos exposed to high glucose show changes in cell...

Full description

Saved in:
Bibliographic Details
Published in:Frontiers in cell and developmental biology 2020-09, Vol.8, p.564561-564561
Main Authors: Valle-Bautista, Rocío, Márquez-Valadez, Berenice, Fragoso-Cabrera, América D., García-López, Guadalupe, Díaz, Néstor Fabián, Herrera-López, Gabriel, Griego, Ernesto, Galván, Emilio J., Arias-Montaño, José-Antonio, Molina-Hernández, Anayansi
Format: Article
Language:English
Subjects:
Cell and Developmental Biology
cerebral cortex development
maternal diabetes
neocortical cytoarchitecture
neocortical function
primary motor cortex
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:Maternal diabetes has been related to low verbal task scores, impaired fine and gross motor skills, and poor performance in graphic and visuospatial tasks during childhood. The primary motor cortex is important for controlling motor functions, and embryos exposed to high glucose show changes in cell proliferation, migration, and differentiation during corticogenesis. However, the existing studies do not discriminate between embryos with or without neural tube defects, making it difficult to conclude whether the reported changes are related to neural tube defects or other anomalies. Furthermore, postnatal effects on central nervous system cytoarchitecture and function have been scarcely addressed. Through molecular, biochemical, morphological, and electrophysiological approaches, we provide evidence of impaired primary motor cerebral cortex lamination and neuronal function in pups from diabetic rats, showing an altered distribution of SATB2, FOXP2, and TBR1, impaired cell migration and polarity, and decreased excitability of deep-layer cortical neurons, suggesting abnormalities in cortico-cortical and extra-cortical innervation. Furthermore, phase-plot analysis of action potentials suggests changes in the activity of potassium channels. These results indicate that high-glucose insult during development promotes complex changes in migration, neurogenesis, cell polarity establishment, and dendritic arborization, which in turn lead to reduced excitability of deep-layer cortical neurons.
ISSN:2296-634X
2296-634X
DOI:10.3389/fcell.2020.564561