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1 Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USA
2 Department of Anatomy, Case Western Reserve University School of Medicine, Cleveland, OH, USA
3 Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USA; Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, USA
* To whom correspondence should be addressed. E-mail: ghaddad{at}ucsd.edu.
Chronic hypoxia, whether continuous (CCH) or intermittent (CIH), occurs in many neonatal pathological conditions such as bronchopulmonary dysplasia (BPD) and obstructive sleep apnea (OSA). In this study, we explored the effect of CCH and CIH on cerebral capillary density and myelination. We subjected CD-1 mice starting at P2 to either CCH 11% oxygen (O2), or CIH 11% O2 (4 minute cycles), for periods of 2 and 4 weeks followed by re-oxygenation for 4 weeks. Mice were deeply anesthetized, perfused and paraffin-embedded coronal brain sections were taken for analysis. Immunocytochemistry for glucose transporter 1 (GLUT-1) was used to assess angiogenesis and Luxol fast blue and fluoromyelin stains were used to assess myelination. Capillary density increased after 2 weeks exposure to CIH and CCH. By 4 weeks, capillary density increased in both CIH and CCH by 25% and 47%, respectively in cortex and by 29% and 44%, respectively in hippocampus (p<0.05). There was a decrease in myelination in the corpus callosum of mice exposed to CIH (75% of control) and CCH (50% of control) (p<0.05). Re-oxygenation reversed the increased capillary density seen in CCH to normoxic values. However, dysmyelination that occurred in CCH-exposed mice did not show any improvement upon re-oxygenation. We conclude that neonatal chronic hypoxia 1) induces brain angiogenesis which is reversible with re-oxygenation and 2) irreversibly reduces the extent of myelination in the corpus callosum. This potential irreversible effect on myelination in early life can therefore have long term and devastating effects.
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