Chronic stress and brain plasticity: Mechanisms underlying adaptive and maladaptive changes and implications for stress-related CNS disorders

NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS

卷:58

Article; Proceedings Paper

Radley, Jason^1,2  Morilak, David^3,4  Viau, Victor⁵  Campeau, Serge⁶ 

[1] Univ Iowa, Dept Psychol & Brain Sci, Iowa City, IA 52242 USA

[2] Univ Iowa, Interdisciplinary Neurosci Program, Iowa City, IA 52242 USA

[3] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA

[4] Univ Texas Hlth Sci Ctr San Antonio, Ctr Biomed Neurosci, San Antonio, TX 78229 USA

[5] Univ British Columbia, Cellular & Physiol Sci, Vancouver, BC V5Z 1M9, Canada

[6] Univ Colorado, Dept Psychol & Neurosci, Boulder, CO 80309 USA

关键词: Chronic stress;    Plasticity;    Prefrontal cortex;    Stress habituation;    Hippocampus;    Amygdala;    Gonadal hormones;   

DOI  :  10.1016/j.neubiorev.2015.06.018

来源: Elsevier

【 摘 要 】

Stress responses entail neuroendocrine, autonomic, and behavioral changes to promote effective coping with real or perceived threats to one's safety. While these responses are critical for the survival of the individual, adverse effects of repeated exposure to stress are widely known to have deleterious effects on health. Thus, a considerable effort in the search for treatments to stress-related CNS disorders necessitates unraveling the brain mechanisms responsible for adaptation under acute conditions and their perturbations following chronic stress exposure. This paper is based upon a symposium from the 2014 International Behavioral Neuroscience Meeting, summarizing some recent advances in understanding the effects of stress on adaptive and maladaptive responses subserved by limbic forebrain networks. An important theme highlighted in this review is that the same networks mediating neuroendocrine, autonomic, and behavioral processes during adaptive coping also comprise targets of the effects of repeated stress exposure in the development of maladaptive states. Where possible, reference is made to the similarity of neurobiological substrates and effects observed following repeated exposure to stress in laboratory animals and the clinical features of stress-related disorders in humans. (C) 2015 Elsevier Ltd. All rights reserved.

【 授权许可】

Free