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Early-life stress impacts the developing hippocampus and primes seizure occurrence: cellular molecular and epigenetic mechanisms

机译:生命早期应激会影响发育中的海马并引发癫痫发作:细胞分子和表观遗传机制

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摘要

Early-life stress includes prenatal, postnatal, and adolescence stress. Early-life stress can affect the development of the hypothalamic-pituitary-adrenal (HPA) axis, and cause cellular and molecular changes in the developing hippocampus that can result in neurobehavioral changes later in life. Epidemiological data implicate stress as a cause of seizures in both children and adults. Emerging evidence indicates that both prenatal and postnatal stress can prime the developing brain for seizures and an increase in epileptogenesis. This article reviews the cellular and molecular changes encountered during prenatal and postnatal stress, and assesses the possible link between these changes and increases in seizure occurrence and epileptogenesis in the developing hippocampus. In addititon, the priming effect of prenatal and postnatal stress for seizures and epileptogenesis is discussed. Finally, the roles of epigenetic modifications in hippocampus and HPA axis programming, early-life stress, and epilepsy are discussed.
机译:生命早期压力包括产前,产后和青春期压力。生命早期应激会影响下丘脑-垂体-肾上腺(HPA)轴的发育,并导致发育中的海马细胞和分子发生变化,从而可能导致生命后期的神经行为发生变化。流行病学数据表明,压力是导致儿童和成人癫痫发作的原因。越来越多的证据表明,产前和产后压力都可以使发育中的大脑为癫痫发作和癫痫发生的增加做好准备。本文回顾了在产前和产后应激过程中遇到的细胞和分子变化,并评估了这些变化与发育中的海马体癫痫发作和癫痫发生增加之间的可能联系。此外,还讨论了产前和产后应激对癫痫发作和癫痫发生的引发作用。最后,讨论了表观遗传修饰在海马和HPA轴编程,早期生活压力和癫痫中的作用。

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