ISSN 1671-3710
CN 11-4766/R
主办:中国科学院心理研究所
出版:科学出版社

心理科学进展 ›› 2016, Vol. 24 ›› Issue (10): 1592-1599.doi: 10.3724/SP.J.1042.2016.01592

• 研究前沿 • 上一篇    下一篇

条件化恐惧复发的动物模型及相关神经机制

付 娟1,2; 郑希耕1; 刘正奎1   

  1. (1中国科学院心理研究所心理健康重点实验室, 北京 100101) (2滨州学院生命科学系, 山东滨州 256603)
  • 收稿日期:2016-01-28 出版日期:2016-10-15 发布日期:2016-10-15
  • 通讯作者: 郑希耕, E-mail: zhengxg@psych.ac.cn
  • 基金资助:

    中国科学院知识创新工程项目(KSCX2-EW-J-8)、中国科学院重点部署项目(KJZD-EW-L04-2)、山东省自然科学基金项目(ZR2015CL025)、滨州市科学技术发展计划项目(2014ZC0328)。

Animal models and related neurobiological mechanisms of conditioned fear relapse

FU Juan1,2; ZHENG Xi-Geng1; LIU Zheng-Kui1   

  1. (1 Key Laboratory of Mental Health, Institute of psychology, Chinese Academy of Science, Beijing 100101, China) (2 Department of Life Science, Binzhou University, Binzhou 256600, China)
  • Received:2016-01-28 Online:2016-10-15 Published:2016-10-15
  • Contact: ZHENG Xi-Geng, E-mail: zhengxg@psych.ac.cn

摘要:

创伤后应激障碍(PTSD)受到国内外普遍关注, 临床上常用的暴露疗法就是基于消退原理, 但经过治疗的患者复发率仍然很高, 这提示抑制复发可能是治疗创伤后应激障碍的关键问题。条件性恐惧复发的动物模型主要包括重建、续新和自发恢复, 但是对续新的研究最多。前人的研究结果表明, 恐惧复发具有异质性, 但海马、前额叶与杏仁核三大脑区或许构成了共同的神经基础。文章从脑区机制及药理干预方面进行了综述, 以期对基础研究和临床诊治提供参考。

关键词: 恐惧复发, 动物模型, 消退, 神经生物学机制

Abstract:

Post-traumatic stress disorder (PTSD) has received widespread concern at home and abroad. Exposure therapy, based on fear extinction, is commonly used in clinical practice. But the recurrence rate is still high after treatment. It suggests that the inhibition of fear relapse may be the key issue in the treatment of PTSD. Animal models of conditioned fear relapse include reinstatement, renewal, and spontaneous recovery, but most of the research has focused on renewal. Previous studies showed that fear relapse has heterogeneity, but the hippocampus, prefrontal cortex and amygdale may constitute common neural substrates. This article reviews brain region mechanisms and pharmacological intervention associated with conditioned fear relapse. It may provide reference for theoretical study and clinical treatment.

Key words: fear relapse, animal models, extinction, neurobiological mechanisms