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Reduction of cortical parvalbumin expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition

Item Type:Article
Title:Reduction of cortical parvalbumin expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition
Creators Name:Scheuer, T. and Auf dem Brinke, E. and Grosser, S. and Wolf, S.A. and Mattei, D. and Sharkovska, Y. and Barthel, P.C. and Endesfelder, S. and Friedrich, V. and Bührer, C. and Vida, I. and Schmitz, T.
Abstract:The inhibitory GABAergic system in the brain is involved in the etiology of various psychiatric problems, including autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and others. These disorders are influenced not only by genetic but also by environmental factors, such as preterm birth, although the mechanisms underlying are not known. In a translational hyperoxia model, exposing mice pups at age P5 to 80% oxygen for 48 hours to mimic a steep rise of oxygen exposure caused by preterm birth from in utero into room air, we documented a persistent reduction of cortical mature parvalbumin expressing interneurons until adulthood. Developmental delay of cortical myelin was observed together with decreased expression of oligodendroglial glial cell-derived neurotrophic factor (GDNF), a factor being involved in interneuronal development. Electrophysiological and morphological properties of remaining interneurons were unaffected. Behavioral deficits were observed for social interaction, learning, and attention. These results elucidate that neonatal oxidative stress can lead to decreased interneuron density and to psychiatric symptoms. The obtained cortical myelin deficit and decreased oligodendroglial GDNF expression indicate an impaired oligodendroglial-interneuronal interplay contributes to interneuronal damage.
Keywords:ADHD, ASD, Cortical Interneurons, GDNF, Oligodendroglial, Oxidative Stress, Preterm Birth, Animals, Mice
Source:Development
ISSN:0950-1991
Publisher:Company of Biologists
Volume:148
Number:20
Page Range:dev.198390
Date:October 2021
Official Publication:https://doi.org/10.1242/dev.198390
PubMed:View item in PubMed

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