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Hyperoxygenation During Mid-Neurogenesis Accelerates Cortical Development in the Fetal Mouse Brain
Franz Markert1, Alexander Storch1,2
1Department of Neurology, University of Rostock, Rostock, Germany.
Frontiers in Cell and Developmental Biology
|April 4, 2022
Summary
Fetal brain hyperoxygenation temporarily boosts neuron growth, accelerating cortical development. However, these effects are transient, with no lasting morphological changes observed post-birth.
Area of Science:
- Neuroscience
- Developmental Biology
- Perinatal Medicine
Background:
- Oxygen tension significantly influences fetal brain development.
- Previous studies show hyperoxygenation increases neuroprecursor cells, affecting brain size.
Purpose of the Study:
- To investigate if fetal brain hyperoxygenation during mid-neurogenesis causes persistent morphological changes.
- To understand the long-term impact of transient hyperoxygenation on cortical development.
Main Methods:
- Controlled fetal brain hyperoxygenation in mice (E14.5-E16.5) using 75% oxygen.
- Analysis of brain development via immunofluorescence staining at multiple embryonic and postnatal stages.
- Assessment of apoptosis and cell proliferation using cleaved caspase 3 and BrdU/EdU labeling.
Main Results:
- Hyperoxygenation accelerated cortical development with increased neuron counts until birth.
- Cortical layer 5 (L5) neuron counts (Ctip2+) transiently increased but normalized by postnatal day 3.5.
- Microglial activation in L5 targeted Ctip2+ neurons, without significant apoptosis, accompanied normalization.
Conclusions:
- Mid-neurogenesis hyperoxygenation causes a transient overshoot of cortical L5 neurons.
- Accelerated cortical development due to hyperoxygenation does not lead to persistent morphological changes.
- Microglial activity may play a role in normalizing neuron populations post-hyperoxygenation.
