即刻消退缺损的原因分析及其神经生物学机制

Immediate extinction deficit:Causes and neurobiological mechanisms

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。

Extinction training that occurs shortly after fear conditioning fails to yield long-term extinction memory,a phenomenon that is known as the immediate extinction deficit(IED).The IED may be linked to levels of stress at the onset of extinction training and event segmentation.Under high levels of stress,the consolidation of extinction memory is impaired,resulting in the IED.Under moderate or low levels of stress,immediate extinction would be effective but susceptible to event segmentation.The neurobiological mechanisms of IED may involve stress-induced activation of the locus coeruleus norepinephrine system,which leads to hyperexcitability of the basolateral amygdala and the subsequent inhibition of activity of the medial prefrontal cortex(i.e.,a region that plays a central role in fear extinction)through synaptic projections.Future studies should consider long-term outcomes of the IED and optimization of the clinical application of immediate extinction.