Glucocorticoids, depression, and mood disorders: structural remodeling in the brain
Glucocorticoids, depression, and mood disorders: structural remodeling in the brain
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DOI：
10.1016/j.metabol.2005.01.008
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发表时间：
2005-05-01
影响因子：
9.8
通讯作者：
McEwen, BS
中科院分区：
文献类型：
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作者：
McEwen, BS
海马体的形成表达了高水平的肾上腺类固醇受体，是一种可塑的大脑结构，对某些类型的学习和记忆很重要。它也容易受到压力和创伤的影响。杏仁核是应激的重要目标，介导与恐惧和强烈情绪相关的生理和行为反应。前额叶皮层在工作记忆和执行功能中起着重要作用，也与学习的消失有关。这三个区域都是应激激素的目标，而压力会加速和加剧情绪障碍。在长期抑郁症中，海马体和前额叶皮层萎缩，而杏仁核在焦虑和情绪障碍中过度活跃，并可能经历结构的双相变化——急性抑郁症时体积增大，长期抑郁症时体积缩小。在急性和慢性应激动物模型中，海马和前额叶皮层的神经元对反复应激的反应表现为萎缩，导致记忆障碍，而杏仁核的神经元则表现为生长反应，导致焦虑和攻击性增加。然而，这些并不一定是“受损”的，可以通过正确的药物治疗。在此背景下讨论了区分压力对脑细胞的保护和损害的机制，(c) 2005 Elsevier Inc.。版权所有。
The hippocampal formation expresses high levels of adrenal steroid receptors and is a malleable brain structure that is important for certain types of learning and memory. It is also vulnerable to the effects of stress and trauma. The amygdala is an important target of stress and mediates physiological and behavioral responses associated with fear and strong emotions. The prefrontal cortex plays an important role in working memory and executive function and is also involved in extinction of learning. All 3 regions are targets of stress hormones, and stress is known to precipitate and exacerbate mood disorders. In long-term depressive illness, the hippocampus and prefrontal cortex undergo atrophy, whereas the amygdala is hyperactive in anxiety and mood disorders and may undergo a biphasic change in structure - increasing in size in acute depression and shrinking on long-term depression. In animal models of acute and chronic stress, neurons in the hippocampus and prefrontal cortex respond to repeated stress by showing atrophy that leads to memory impairment, whereas neurons in amygdala show a growth response that leads to increased anxiety and aggression. Yet, these are not necessarily "damaged" and may be treatable with the right medications. The mechanisms that distinguish between protection and damage of brain cells from stress are discussed in this context, (c) 2005 Elsevier Inc. All rights reserved.