Laboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Neuropharmacology. 2012 Jan;62(1):3-12. doi: 10.1016/j.neuropharm.2011.07.014. Epub 2011 Jul 27.
The brain is the central organ of stress and adaptation to stress because it perceives and determines what is threatening, as well as the behavioral and physiological responses to the stressor. The adult, as well as developing brain, possess a remarkable ability to show reversible structural and functional plasticity in response to stressful and other experiences, including neuronal replacement, dendritic remodeling, and synapse turnover. This is particularly evident in the hippocampus, where all three types of structural plasticity have been recognized and investigated, using a combination of morphological, molecular, pharmacological, electrophysiological and behavioral approaches. The amygdala and the prefrontal cortex, brain regions involved in anxiety and fear, mood, cognitive function and behavioral control, also show structural plasticity. Acute and chronic stress cause an imbalance of neural circuitry subserving cognition, decision making, anxiety and mood that can increase or decrease expression of those behaviors and behavioral states. In the short term, such as for increased fearful vigilance and anxiety in a threatening environment, these changes may be adaptive; but, if the danger passes and the behavioral state persists along with the changes in neural circuitry, such maladaptation may need intervention with a combination of pharmacological and behavioral therapies, as is the case for chronic or mood anxiety disorders. We shall review cellular and molecular mechanisms, as well as recent work on individual differences in anxiety-like behavior and also developmental influences that bias how the brain responds to stressors. Finally, we suggest that such an approach needs to be extended to other brain areas that are also involved in anxiety and mood. This article is part of a Special Issue entitled 'Anxiety and Depression'.
大脑是应激和适应应激的中枢器官，因为它感知和确定什么是威胁，以及对应激源的行为和生理反应。成人和发育中的大脑都具有显著的能力，能够对压力和其他经历产生可逆的结构和功能可塑性，包括神经元替代、树突重塑和突触更替。这在海马体中尤为明显，在海马体中，已经使用形态学、分子学、药理学、电生理学和行为学方法的组合，识别和研究了所有三种类型的结构可塑性。参与焦虑和恐惧、情绪、认知功能和行为控制的杏仁核和前额叶皮层也表现出结构可塑性。急性和慢性应激会导致认知、决策、焦虑和情绪的神经回路失衡，从而增加或减少这些行为和行为状态的表达。在短期内，例如在威胁环境中增加恐惧警惕性和焦虑，这些变化可能是适应性的；但是，如果危险过去，并且行为状态伴随着神经回路的变化持续存在，这种适应不良可能需要结合药理学和行为疗法进行干预，就像慢性或情绪焦虑障碍一样。我们将回顾细胞和分子机制，以及最近关于焦虑样行为个体差异的研究工作，以及影响大脑对应激源反应方式的发育影响。最后，我们建议这种方法需要扩展到其他也参与焦虑和情绪的大脑区域。本文是题为“焦虑和抑郁”的特刊的一部分。
