Neurogenesis and maturation in neonatal brain injury.
Neurogenesis and maturation in neonatal brain injury.
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DOI：
10.1016/j.clp.2013.10.007
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发表时间：
2014-03
影响因子：
2.1
通讯作者：
Vaccarino FM
中科院分区：
文献类型：
--
作者：
Salmaso N;Tomasi S;Vaccarino FM
早产的发生率正在上升。早产的结果可能差异很大，从完全正常的发育到严重的神经缺陷，大多数儿童表现出轻度至中度的认知延迟，神经精神疾病的发病率增加，如焦虑，注意力缺陷多动和自闭症谱系障碍。已经提出了几种动物模型来研究早产的后果，其中最有前途的是小鼠的慢性围产期缺氧，其概括了认知障碍，功能随时间的部分恢复以及环境丰富后的改善。在动物模型中，慢性围产期缺氧的一个主要后果是星形胶质细胞、寡树突细胞和神经元的成熟延迟，特别是大脑皮层中抑制性小白蛋白中间神经元。虽然延迟的成熟可以被视为适应性的，因为它允许延长的神经发生和突触可塑性，但它也导致髓鞘形成减少，神经元生长异常，并且可能损害电活动的抑制性调节。值得注意的是，增加细胞成熟的干预措施，如环境富集，可以逆转其中一些细胞和行为缺陷。
The incidence of preterm birth is on the rise. The outcome of premature birth can vary widely, spanning completely normal development to severe neurological deficits, with a majority of children showing mild to moderate cognitive delay and increased incidence of neuropsychiatric conditions such as anxiety, attention deficit hyperactivity and autism spectrum disorders. Several animal models have been proposed to study the consequences of prematurity, one of the most promising being chronic perinatal hypoxia in mouse, which recapitulates the cognitive impairment, the partial recovery of function over time and the improvement after environmental enrichment. A major consequence of chronic perinatal hypoxia in animal models is delayed maturation of astrocytes, oligodendocytes and neurons, particularly inhibitory parvalbumin interneurons in the cerebral cortex. While delayed maturation can be seen as adaptive in that it allows prolonged neurogenesis and synaptic plasticity, it also leads to decreased myelination, aberrant neuron growth and likely impaired inhibitory regulation of electrical activity. Remarkably, interventions that increase cell maturation, such as environmental enrichment, reverse some of these cellular and behavioral deficits.
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DOI：
10.1073/pnas.250471697
发表时间：
2000-12-05
影响因子：
11.1
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