Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder.
Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder.
复制标题
创伤后应激障碍中未能回忆灭绝记忆的神经生物学基础。
DOI：
10.1016/j.biopsych.2009.06.026
复制
发表时间：
2009-12-15
影响因子：
10.6
通讯作者：
Rauch, Scott L.
中科院分区：
文献类型：
--
作者：
Milad, Mohammed R.;Pitman, Roger K.;Ellis, Cameron B.;Gold, Andrea L.;Shin, Lisa M.;Lasko, Natasha B.;Zeidan, Mohamed A.;Handwerger, Kathryn;Orr, Scott P.;Rauch, Scott L.
关键词：
创伤后应激障碍（PTSD）的一个临床特征是对与创伤事件相关的刺激的恐惧反应持续升高。本文的目的是确定恐惧反应的消退是否在 PTSD 中受损，以及这种损害是否与已知参与恐惧消退的大脑区域（即杏仁核、海马体、腹内侧前额叶皮层 (vmPFC) 和背侧前扣带皮层 (dACC)）的功能失调有关。 16 名被诊断患有 PTSD 的个体和 15 名遭受创伤的非 PTSD 对照组 (TENC) 在 3T fMRI 扫描仪中接受了为期两天的恐惧条件反射和消除方案。第一天进行条件反射和消退训练。第二天进行消退回忆（或消退记忆）测试（在没有电击的情况下出现条件刺激）。在整个实验过程中对皮肤电导反应（SCR）进行评分，作为条件反应的指标。 SCR 数据显示，在第一天条件性恐惧的获得和消退过程中，各组之间没有显着差异。然而，在第二天，PTSD 受试者表现出消退记忆的回忆受损。功能磁共振成像数据分析显示，在第一天的消退学习过程中，PTSD 组的杏仁核激活程度更高。在消退回忆过程中，PTSD 组观察到海马和 vmPFC 的激活较少，而 dACC 的激活较多。所有受试者的消退记忆强度与消退回忆测试期间海马体和 vmPFC 的激活相关。这些发现支持了创伤后应激障碍（PTSD）中恐惧消退受到损害的假设。他们进一步表明，介导恐惧消退学习（尤其是回忆）的大脑结构激活功能失调是造成这种损伤的原因。
A clinical characteristic of posttraumatic stress disorder (PTSD) is persistently elevated fear responses to stimuli associated with the traumatic event. The objective herein is to determine whether extinction of fear responses is impaired in PTSD and whether such impairment is related to dysfunctional activation of brain regions known to be involved in fear extinction, viz., amygdala, hippocampus, ventromedial prefrontal cortex (vmPFC), and dorsal anterior cingulate cortex (dACC). Sixteen individuals diagnosed with PTSD and 15 trauma-exposed non-PTSD controls (TENCs) underwent a two-day fear conditioning and extinction protocol in a 3T fMRI scanner. Conditioning and extinction training were conducted on day 1. Extinction recall (or extinction memory) test was conducted on day 2 (extinguished conditioned stimuli presented in the absence of shock). Skin conductance response (SCR) was scored throughout the experiment as an index of the conditioned response. SCR data revealed no significant differences between groups during acquisition and extinction of conditioned fear on day 1. On day 2, however, PTSD subjects showed impaired recall of extinction memory. Analysis of fMRI data showed greater amygdala activation in the PTSD group during day 1 extinction learning. During extinction recall, lesser activation in hippocampus and vmPFC, and greater activation in dACC, was observed in the PTSD group. The magnitude of extinction memory across all subjects was correlated with activation of hippocampus and vmPFC during extinction recall testing. These findings support the hypothesis that fear extinction is impaired in PTSD. They further suggest that dysfunctional activation in brain structures that mediate fear extinction learning, and especially its recall, underlie this impairment.
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DOI：
10.1523/jneurosci.2021-06.2006
发表时间：
2006-09-13
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Kalisch R;Korenfeld E;Stephan KE;Weiskopf N;Seymour B;Dolan RJ
通讯作者：
Dolan RJ
影响因子：
6.9
作者：
Bremner, JD;Vermetten, E;Charney, DS
通讯作者：
Charney, DS
影响因子：
10.6
作者：
Lanius, RA;Williamson, PC;Menon, RS
通讯作者：
Menon, RS
影响因子：
10.6
作者：
Liberzon, I;Taylor, SF;Fig, LM
通讯作者：
Fig, LM
影响因子：
5.7
作者：
Dale, AM;Fischl, B;Sereno, MI
通讯作者：
Sereno, MI