JOURNAL/mgres/04.03/01612956-990000000-00073/figure1/v/2026-01-23T123057Z/r/image-tiff Defects in myelination impair nerve impulse conduction and functional connectivity, which could lead to cognitive, behavioral and motor deficits in various neurological disorders. Adequate oxygen delivery is vital for brain development, while hypoxia in newborns tends to result in developmental deficiencies in myelination of the brain. The disruption of oligodendrocytes and their progenitor cells caused by hypoxia has been well researched. Nonetheless, the impairing dynamic myelination process is still unclear. Utilizing zebrafish as a model, we established hypoxia via cobalt chloride exposure or low oxygen (8%) incubation. Hypoxia significantly reduced oligodendrocyte progenitor cell numbers in the dorsal spinal cord, impaired migration velocity and suppressed proliferation. Myelination deficits were evident through decreased myelin sheath segment intensity in Tg(MBP:eGFP-CAAX) larvae. Time-lapse imaging revealed compromised dynamic myelination by individual oligodendrocytes under hypoxia, with fewer sheaths and reduced extension rates. Mechanistically, hypoxia elevated reactive oxygen species levels and disrupted mitochondrial membrane potential in cultured rat oligodendrocyte progenitor cells. Nanoscale magnesium hydride, a hydrogen-releasing agent, attenuated these effects. In vivo , magnesium hydride treatment rescued oligodendrocyte progenitor cell numbers and enhanced myelinogenesis capacity in hypoxic zebrafish. These findings demonstrate that magnesium hydride mitigates hypoxia-induced oxidative stress and mitochondrial dysfunction, thereby alleviating myelination deficits.
Li et al. (Fri,) studied this question.