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Neonatal Hyperoxia Perturbs Neuronal Development in the Cerebellum
Till Scheuer1,2,3, Yuliya Sharkovska4,5, Victor Tarabykin5
1Department for Neonatology, Charité University Medical Center, Berlin, Germany. Till.Scheuer@charite.de.
Molecular Neurobiology
|May 27, 2017
Summary
Postnatal oxygen toxicity in newborns can damage cerebellar neurons, potentially explaining developmental issues in preterm infants. This study shows hyperoxia impairs granule and Purkinje cell development, leading to long-term neurological deficits.
Area of Science:
- Neuroscience
- Developmental Biology
- Neonatal Research
Background:
- Preterm infants often experience impaired postnatal brain development, leading to neurological deficits.
- Cerebellar maldevelopment is increasingly linked to psychomotor impairments in former preterm infants, but causes remain unclear.
Purpose of the Study:
- To investigate the effects of neonatal hyperoxia on cerebellar granule cell precursors (GCPs) and Purkinje cells (PCs).
- To define the postnatal and long-term damage caused by hyperoxia in the developing cerebellum.
Main Methods:
- Newborn rats were exposed to 80% oxygen from postnatal day 6 to 7.
- Immunohistochemistry, qPCR, and Western blots were used to assess cell proliferation, apoptosis, neuronal markers, and SHH signaling.
- Dendrite outgrowth of Purkinje cells was analyzed using immunostainings and Golgi staining.
Main Results:
- Hyperoxia decreased GCP proliferation and increased apoptosis, with downregulated neuronal markers (Pax6, Tbr2, Prox1, NeuN) observed long-term.
- Reduced Sonic hedgehog (SHH) signaling was noted, coinciding with decreased CyclinD2 and Hes1 expression.
- Granule cell injury was associated with hampered Purkinje cell maturation, including delayed dendrite formation and impaired branching.
Conclusions:
- Neonatal hyperoxia induces significant damage to cerebellar granule cells and Purkinje cells.
- This damage inhibits neuronal development and function, suggesting postnatal oxygen toxicity as a potential cause of cerebellar maldevelopment in preterm infants.
