Program in Neurodevelopment and Regeneration, Yale University, New Haven, Connecticut, USA.
Center for Neuroscience Research, Children's National Medical Center, Washington, DC, USA.
Nat Neurosci. 2014 Mar;17(3):341-6. doi: 10.1038/nn.3604. Epub 2014 Feb 25.
Every year in the United States, an estimated 500,000 babies are born preterm (before 37 completed weeks of gestation), and this number is rising, along with the recognition of brain injuries due to preterm delivery. A common underlying pathogenesis appears to be perinatal hypoxia induced by immature lung development, which causes injury to vulnerable neurons and glia. Abnormal growth and maturation of susceptible cell types, particularly neurons and oligodendrocytes, in preterm babies with very low birth weight is associated with decreased cerebral and cerebellar volumes and increases in cerebral ventricular size. Here we reconcile these observations with recent studies using models of perinatal hypoxia that show perturbations in the maturation and function of interneurons, oligodendrocytes and astroglia. Together, these findings suggest that the global mechanism by which perinatal hypoxia alters development is through a delay in maturation of affected cell types, including astroglia, oligodendroglia and neurons.
每年在美国，估计有 50 万名婴儿早产（在妊娠 37 周之前），而且这个数字还在上升，同时也认识到了由于早产而导致的脑损伤。一种常见的潜在发病机制似乎是由于不成熟的肺部发育引起的围产期缺氧，这会导致脆弱的神经元和神经胶质细胞受损。极低出生体重的早产儿中，易感细胞类型（特别是神经元和少突胶质细胞）的异常生长和成熟与脑和小脑体积减小以及脑室增大有关。在这里，我们将这些观察结果与最近使用围产期缺氧模型的研究结果进行了调和，这些研究表明，神经元、少突胶质细胞和星形胶质细胞的成熟和功能受到干扰。这些发现表明，围产期缺氧改变发育的整体机制是通过延迟受影响的细胞类型（包括星形胶质细胞、少突胶质细胞和神经元）的成熟。
