Abstract
SummaryAimsNeonatal hypoxia–ischemia (H/I) results in gray and white matter injury, characterized by neuronal loss, failure of neural network formation, retarded myelin formation, and abnormal accumulation of oligodendrocyte progenitor cells (OPCs). These changes lead to severe neurological deficits and mortality. Sublethal hypoxic preconditioning (HPC) can protect the developing brain against H/I. However, limited evidence is available concerning its effect on white matter injury.MethodsIn this study, P6 neonatal Sprague‐Dawley rats were subjected to normoxic (21% O2) or HPC (7.8% O2) for 3 hours followed 24 hours later by H/I brain injury. Neurological deficits were assessed by gait, righting reflex, foot fault, and Morris water maze tests. Compound action potential of the corpus callosum was recorded 35 days after surgery, and the correlation between axon myelination and neurological function was determined.ResultsHypoxic preconditioning significantly attenuated H/I brain injury at 7 days and remarkably improved both sensorimotor and cognitive functional performances up to 35 days after H/I. HPC‐afforded improvement in long‐term neurological outcomes was attributable, at least in part, to restoration of the differentiation and maturation capacity in oligodendrocyte progenitor cells, amelioration of microglia/macrophage activation and neuroinflammation, and continuation of brain development after H/I.ConclusionsHypoxic preconditioning restores white matter repair, development, and functional integrity in developing brain after H/I brain injury.
Highlights
Perinatal hypoxic/ischemic (H/I) brain injury, induced by insuffi‐ cient supply of oxygen and glucose to the brain,[1] occurs in 3 per 1000 preterm infants (
To minimize neurodevelopmental impairments, it is critical that the survival and maturation of late oligodendrocyte progenitors be maintained to facilitate the devel‐ opment of myelin and to rebuild new circuit connections to restore axonal conductive sensitivity in neonates after H/I brain injury.[14]
Our results suggest that hypoxic preconditioning (HPC) promotes long‐term functional recovery of sensorimotor and cognitive deficits by partially rehabilitating the ab‐ normal development of brain parenchyma by revitalizing oligoden‐ drocyte progenitor cell (OPC) maturation and suppressing excessive microglia activation
Summary
State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China. Summary Aims: Neonatal hypoxia–ischemia (H/I) results in gray and white matter injury, char‐ acterized by neuronal loss, failure of neural network formation, retarded myelin for‐ mation, and abnormal accumulation of oligodendrocyte progenitor cells (OPCs). These changes lead to severe neurological deficits and mortality. Sublethal hypoxic preconditioning (HPC) can protect the developing brain against H/I. Results: Hypoxic preconditioning significantly attenuated H/I brain injury at 7 days and remarkably improved both sensorimotor and cognitive functional performances up to 35 days after H/I. Conclusions: Hypoxic preconditioning restores white matter repair, development, and functional integrity in developing brain after H/I brain injury.
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