ISSN 1671-3710
CN 11-4766/R

心理科学进展 ›› 2021, Vol. 29 ›› Issue (1): 150-159.doi: 10.3724/SP.J.1042.2021.00150

• 研究前沿 • 上一篇    下一篇


王红波(), 关旭旭, 李梓萌   

  1. 河南大学认知、脑与健康研究所; 河南大学心理与行为研究所; 河南大学教育科学学院, 开封 475004
  • 收稿日期:2019-11-18 出版日期:2021-01-15 发布日期:2020-11-23
  • 通讯作者: 王红波
  • 基金资助:
    * 教育部人文社会科学研究项目(20YJC190019)

Immediate extinction deficit: Causes and neurobiological mechanisms

WANG Hongbo(), GUAN Xuxu, LI Zimeng   

  1. School of Educational Science, Henan University, Kaifeng 475004, China
    Institute of Cognition, Brain and Health, Henan University, Kaifeng 475004, China; Institute of Psychology and Behavior, Henan University, Kaifeng 475004, China; School of Educational Science, Henan University, Kaifeng 475004, China
  • Received:2019-11-18 Online:2021-01-15 Published:2020-11-23
  • Contact: WANG Hongbo


即刻消退缺损(immediate extinction deficit, IED)是指在条件性恐惧习得后, 立即进行的消退训练不能长期抑制恐惧记忆的现象。IED可能与消退起始时的应激水平和事件分割等因素有关。在高应激水平下, 消退记忆的巩固受损导致IED; 而在中等或较低的应激水平条件下, 即刻消退有效但效果可能容易受事件分割的影响。IED的神经生物学机制涉及应激激活蓝斑去甲肾上腺素能系统, 去甲肾上腺素引起杏仁核基底外侧核(basolateral amygdala, BLA)过度兴奋, 然后BLA通过投射突触抑制在恐惧消退中起核心作用的内侧前额叶神经元的活动。未来研究应注意即刻消退缺损引起的长期后果, 并深入探讨如何优化即刻消退在临床上的应用。

关键词: 条件性恐惧, 即刻消退, 应激水平, 事件分割


Fear memories formed in traumatic experience is pathological basis of stress-related disorders. New memories initially persist in a fragile state and are susceptible to being disrupted by behavioral or pharmacological treatments. Exposure therapy based on extinction is a common treatment for pathological fear. However, extinction training that occurs shortly after fear conditioning is less effective than delayed extinction training in yielding long-term extinction memory, a phenomenon that is known as immediate extinction deficit (IED). The IED may be linked to levels of stress and emotional arousal at the onset of extinction training and event segmentation. If the stress and emotional arousal levels are high at the outset of extinction training, the outcomes of immediate extinction are not influenced by context change or event boundary between fear conditioning and extinction (i.e. event segmentation), but rather mainly affected by the high stress state that can impair the consolidation of extinction memory, resulting in IED. When the levels of stress and emotional arousal are moderate before the onset of extinction training, there is no difference between immediate extinction and delayed extinction, and both of them couldn’t prevent fear relapse. When the stress and emotional arousal levels are low at the time of extinction intervention, the early extinction was more effective than delayed extinction intervention, which could disrupt the consolidation of fear memory and prevent the return of fear. In addition, under moderate or low stress levels, the effect of immediate extinction would be also susceptible to event segmentation. That is, if there is a clear event boundary between fear acquisition and extinction, the event boundary may guide selective consolidation to prioritize the consolidation of emotional information in memory (fear memory) -- at the expense of related but conflicting information (extinction memory) experienced shortly thereafter, leading to IED; if without this event boundary, immediate extinction may retroactively interfere with the consolidation of fear memories and prevent the deficit; but the evidence for this is not yet sufficient. In addition, results from human fear conditioning suggest that the IED phenomenon is not inevitable, even though the electric shock was calibrated to be at the same level deemed “highly annoying but not painful” by each participant. Explanations for this may be that people's criterion for the feeling “highly annoying but not painful” has varied greatly, resulting in the actual stress and emotional arousal level of each participant is different, that is, not all participant are in a high arousal state, therefore IED phenomenon is unstable.
The infralimbic (IL) that is a subdivision of the medial prefrontal cortex (mPFC) plays a key role in the consolidation and retrieval of extinction memory. The basolateral amygdala (BLA) and mPFC form strong reciprocal synaptic connections that play a key role in acquisition and extinction of fear memories. Fear extinction depends on the activities in these two projection pathways, BLA-IL and IL-BLA, which are trade-off. The neurobiological mechanisms of IED may involve that: (1) stress-induced activation of the locus coeruleus norepinephrine (LC-NE) system evokes extensive release of NE in BLA through LC-projecting neurons, leading to hyperactivity of BLA; and (2) stress-activated corticotropin releasing factor (CRF) system in BLA triggers the release of CRF that binds G-protein-coupled receptors (CRFR1), resulting in hyperexcitability of BLA; then overactive BLA inputs suppress the activity of IL via feedforward inhibition of projection neurons, which further impair the consolidation of extinction memories, causing IED. Future studies should examine whether the IED is just an aberration or early extinction acts as a secondary trauma which can continually damage the ability to extinguish fear memory, instead, contributes to the development of stress-related disorders, and explore how to optimize the clinical application of immediate extinction. 

Key words: fear conditioning, immediate extinction, stress level, event segmentation