Hypoxia and brain development
Hypoxia and brain development
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DOI：
10.1016/0301-0082(96)00007-x
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发表时间：
1996-05
影响因子：
6.7
通讯作者：
C. Nyakas;Bauke Buwald;P. Luiten
中科院分区：
文献类型：
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作者：
C. Nyakas;Bauke Buwald;P. Luiten
从胎儿早期到衰老的整个生命周期中，缺氧都会威胁到大脑功能。本综述比较了胎儿慢性缺氧和新生儿缺氧对几种行为范式（包括新奇诱导的自发行为和学习行为）的短期、长期和整个生命周期的影响。此外，它还表明，围产期缺氧是衰老过程中神经退行性变以及认知和其他行为下降的额外威胁。产前缺氧会引起胆碱能和血清素能纤维向海马和新皮质内生长的暂时延迟，并导致衰老过程中 5-HT-ir 轴突的神经变性增强。新生儿缺氧抑制海马 ChAT 活性并上调出生后早期海马中 3 H-QNB 和 3 H-哌仑西平结合的毒蕈碱受体位点。轴突树枝化和突触前和突触后胆碱能功能的改变发展可能是解释行为缺陷的重要潜在机制。就围产期缺氧的细胞机制而言，我们的主要目的是通过药物干预和测量 Ca2+ 结合蛋白免疫表达的发育来研究发育神经元中 Ca2+ 稳态的假定重要性。我们评估尼莫地平（一种 L 型钙通道阻滞剂）可预防或减轻围产期缺氧的不良行为和神经化学影响，同时增强 ir-Ca2+ 结合蛋白的产后早期发育。这些结果在大脑发育、缺氧和缺血的不同相关研究领域的背景下进行了讨论。
Hypoxia threatens brain function during the entire life-span starting from early fetal age up to senescence. This review compares the short-term, long-term and life-spanning effects of fetal chronic hypoxia and neonatal anoxia on several behavioural paradigms including novelty-induced spontaneous and learning behaviours. Furthermore, it reveals that perinatal hypoxia is an additional threat to neurodegeneration and decline of cognitive and other behaviours during the aging process. Prenatal hypoxia evokes a temporary delay of ingrowth of cholinergic and serotonergic fibres into the hippocampus and neocortex, and causes an enhanced neurodegeneration of 5-HT-ir axons during aging. Neonatal anoxia suppresses hippocampal ChAT activity and up-regulates muscarinic receptor sites for3H-QNB and3H-pirenzepine binding in the hippocampus in the early postnatal age. The altered development of axonal arborizatio n and pre- and postsynaptic cholinergic functions may be an important underlying mechanism to explain the behavioural deficits. As far as the cellular mechanisms of perinatal hypoxia is concerned, our primary aim was to study the putative importance of Ca2+homeostasis of developing neurons by means of pharmacological interventions and by measuring the development of immunoexpression of Ca2+-binding proteins. We assessed that nimodipine, an L-type calcium channel blocker, prevented or attenuated the adverse behavioural and neurochemical effects of perinatal hypoxias, while it enhanced the early postnatal development of ir-Ca2+-binding proteins. The results are discussed in the context of different related research areas on brain development and hypoxia and ischaemia.