Psychobiology of persistent antisocial behavior: Stress, early vulnerabilities and the attenuation hypothesis
Psychobiology of persistent antisocial behavior: Stress, early vulnerabilities and the attenuation hypothesis
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DOI：
10.1016/j.neubiorev.2005.08.002
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发表时间：
2006-01-01
影响因子：
8.2
通讯作者：
Susman, EJ
中科院分区：
文献类型：
--
作者：
Susman, EJ
在大脑发育的敏感的产前、产后和幼儿期经历的压力可能对发育中的生物系统产生破坏性后果。压力施加的早期身体的脆弱性和不利的照顾环境中提出设置运动的早期前兆，后来持续的反社会行为。本报告的目的是提出一个综合的理论观点的潜在机制参与发展的持续性反社会行为的早期压力源和压力的神经内分泌学的重点。压力系统的内分泌生理的衰减被认为是持续性反社会行为的关键机制。杏仁核被认为是连接主观体验、情绪学习、大脑发育和压力生理学的结构/过程。早期脆弱性之后皮质醇水平的降低被认为是持续反社会行为的风险标志。(c)2005爱思唯尔有限公司保留所有权利。
Stress experienced during the sensitive prenatal, postnatal and early childhood periods of brain development can have damaging consequences for developing biological systems. Stressors imposed by early physical vulnerabilities and an adverse care giving environment is proposed to set in motion early precursors of later persistent antisocial behavior. The purpose of this report is to present an integrated theoretical perspective of potential mechanisms involved in the development of persistent antisocial behavior with an emphasis on early stressors and the neuroendocrinology of stress. The attenuation of endocrine physiology of the stress system is considered a key mechanism involved in persistent antisocial behavior. The amygdala is considered a structure/process linking subjective experiences, emotional learning, brain development and stress physiology. Attenuated cortisol level subsequent to early vulnerabilities is considered a risk marker for persistent antisocial behavior. (c) 2005 Elsevier Ltd. All rights reserved.