Neural control of chronic stress adaptation.
Neural control of chronic stress adaptation.
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DOI：
10.3389/fnbeh.2013.00061
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发表时间：
2013
影响因子：
3
通讯作者：
Herman JP
中科院分区：
文献类型：
--
作者：
Herman JP
压力启动了适应过程，使生物体能够在生理上科普长期或间歇性暴露于真实的或感知到的威胁。这种反应的一个主要组成部分是下丘脑-垂体-肾上腺皮质（HPA）轴反复激活糖皮质激素分泌，这促进了包括大脑在内的广泛器官系统中能量的重新分配。糖皮质激素分泌的长期或累积增加可减少由增强的应激反应提供的益处，并最终变得适应不良。压力的长期影响通过习惯化过程来控制，习惯化过程在重复暴露于同型压力源时减少HPA轴反应，并可能限制长期糖皮质激素分泌的有害作用。习惯化受边缘系统应激调节位点的调节，并且至少部分地依赖于糖皮质激素反馈。慢性压力也会使人对新刺激的反应变得敏感。虽然致敏在保持应对新威胁的反应灵活性方面可能很重要，但它也可能增加糖皮质激素对大脑和身体的累积影响。最后，不可预测的或严重的压力暴露可能会导致HPA轴的长期和持久的失调，可能是由于边缘系统对压力效应通路的控制改变。与压力相关的疾病，如抑郁症和创伤后应激障碍，伴随着糖皮质激素失衡和边缘回路的结构/功能改变，类似于慢性压力后所见，这表明对压力信息的不适当处理可能是病理过程的一部分。
Stress initiates adaptive processes that allow the organism to physiologically cope with prolonged or intermittent exposure to real or perceived threats. A major component of this response is repeated activation of glucocorticoid secretion by the hypothalamo-pituitary-adrenocortical (HPA) axis, which promotes redistribution of energy in a wide range of organ systems, including the brain. Prolonged or cumulative increases in glucocorticoid secretion can reduce benefits afforded by enhanced stress reactivity and eventually become maladaptive. The long-term impact of stress is kept in check by the process of habituation, which reduces HPA axis responses upon repeated exposure to homotypic stressors and likely limits deleterious actions of prolonged glucocorticoid secretion. Habituation is regulated by limbic stress-regulatory sites, and is at least in part glucocorticoid feedback-dependent. Chronic stress also sensitizes reactivity to new stimuli. While sensitization may be important in maintaining response flexibility in response to new threats, it may also add to the cumulative impact of glucocorticoids on the brain and body. Finally, unpredictable or severe stress exposure may cause long-term and lasting dysregulation of the HPA axis, likely due to altered limbic control of stress effector pathways. Stress-related disorders, such as depression and PTSD, are accompanied by glucocorticoid imbalances and structural/ functional alterations in limbic circuits that resemble those seen following chronic stress, suggesting that inappropriate processing of stressful information may be part of the pathological process.