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应激反应与围产期重编程:解读(非)适应性策略

Stress Response and Perinatal Reprogramming: Unraveling (Mal)adaptive Strategies.

作者信息

Musazzi Laura, Marrocco Jordan

机构信息

Laboratorio di Neuropsicofarmacologia e Neurogenomica Funzionale, Dipartimento di Scienze Farmacologiche e Biomolecolari and CEND, Università degli Studi di Milano, 20133 Milano, Italy.

Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY 10065, USA.

出版信息

Neural Plast. 2016;2016:6752193. doi: 10.1155/2016/6752193. Epub 2016 Mar 16.

DOI:10.1155/2016/6752193
PMID:27057367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4812483/
Abstract

Environmental stressors induce coping strategies in the majority of individuals. The stress response, involving the activation of the hypothalamic-pituitary-adrenocortical axis and the consequent release of corticosteroid hormones, is indeed aimed at promoting metabolic, functional, and behavioral adaptations. However, behavioral stress is also associated with fast and long-lasting neurochemical, structural, and behavioral changes, leading to long-term remodeling of glutamate transmission, and increased susceptibility to neuropsychiatric disorders. Of note, early-life events, both in utero and during the early postnatal life, trigger reprogramming of the stress response, which is often associated with loss of stress resilience and ensuing neurobehavioral (mal)adaptations. Indeed, adverse experiences in early life are known to induce long-term stress-related neuropsychiatric disorders in vulnerable individuals. Here, we discuss recent findings about stress remodeling of excitatory neurotransmission and brain morphology in animal models of behavioral stress. These changes are likely driven by epigenetic factors that lie at the core of the stress-response reprogramming in individuals with a history of perinatal stress. We propose that reprogramming mechanisms may underlie the reorganization of excitatory neurotransmission in the short- and long-term response to stressful stimuli.

摘要

环境应激源会在大多数个体中引发应对策略。应激反应,包括下丘脑 - 垂体 - 肾上腺皮质轴的激活以及随之而来的皮质类固醇激素的释放,实际上旨在促进代谢、功能和行为适应。然而,行为应激也与快速且持久的神经化学、结构和行为变化相关,导致谷氨酸传递的长期重塑,并增加对神经精神疾病的易感性。值得注意的是,子宫内和出生后早期的早期生活事件会引发应激反应的重新编程,这通常与应激恢复力的丧失以及随之而来的神经行为(不良)适应有关。事实上,已知早年的不良经历会在易受影响的个体中诱发长期的应激相关神经精神疾病。在此,我们讨论行为应激动物模型中兴奋性神经传递和脑形态的应激重塑的最新发现。这些变化可能由表观遗传因素驱动,而表观遗传因素是有围产期应激史个体应激反应重新编程的核心。我们提出重新编程机制可能是短期和长期应激刺激下兴奋性神经传递重组的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/476f/4812483/3f992f34ab9d/NP2016-6752193.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/476f/4812483/4cec22d6ccf9/NP2016-6752193.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/476f/4812483/3f992f34ab9d/NP2016-6752193.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/476f/4812483/4cec22d6ccf9/NP2016-6752193.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/476f/4812483/3f992f34ab9d/NP2016-6752193.002.jpg

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