Psychobiology of persistent antisocial behavior: Stress, early vulnerabilities and the attenuation hypothesis

被引:249
|
作者
Susman, EJ [1 ]
机构
[1] Penn State Univ, Dept Biobehav Hlth, Biobehav Transit Lab, University Pk, PA 16802 USA
来源
关键词
persistent antisocial behavior; stress physiology; cortisol; early learning; brain development;
D O I
10.1016/j.neubiorev.2005.08.002
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
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.
引用
收藏
页码:376 / 389
页数:14
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