Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany; International Max Planck Research School for Translational Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Trends Neurosci. 2020 Jun;43(6):394-405. doi: 10.1016/j.tins.2020.03.008. Epub 2020 Apr 15.
A number of prenatal experiences are associated with adverse outcomes after birth, ranging from cardiovascular problems to psychiatric disease. Prenatal stress is associated with neurodevelopmental alterations that persist after birth and manifest at the behavioral level, for example, increased fearfulness, and at the physiological one, that is, brain structural and functional changes. Understanding the mechanisms that drive these lasting effects may help in preventing long-term negative outcomes of prenatal stress. Elevated glucocorticoid signaling in utero may be one of the key mediators of prenatal stress effects on the offspring. In this review, we summarize how prenatal glucocorticoids may impact the activity of the fetal hypothalamic-pituitary-adrenal (HPA) axis, disrupt neurodevelopmental processes and alter the epigenetic landscape of the fetus. We also discuss the need to take into consideration the interaction of these processes with the offspring's genetic landscape.
许多产前经历与出生后的不良后果有关,范围从心血管问题到精神疾病。产前应激与神经发育改变有关,这些改变在出生后持续存在,并表现在行为层面,例如增加恐惧,以及在生理层面,即大脑结构和功能的变化。了解驱动这些持久影响的机制可能有助于预防产前应激的长期负面后果。子宫内升高的糖皮质激素信号可能是产前应激对子代影响的关键介质之一。在这篇综述中,我们总结了产前糖皮质激素如何影响胎儿下丘脑-垂体-肾上腺 (HPA) 轴的活性,破坏神经发育过程并改变胎儿的表观遗传景观。我们还讨论了需要考虑这些过程与后代遗传景观的相互作用。