| 睡眠对恐惧学习的影响及其认知神经机制 |
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| 引用本文： | 张婕,张火垠,李红,雷怡. 睡眠对恐惧学习的影响及其认知神经机制[J]. 心理科学进展, 2023, 31(4): 631-640. DOI: 10.3724/SP.J.1042.2023.00631 |
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| 作者姓名： | 张婕 张火垠 李红 雷怡 |
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| 作者单位： | 1.四川师范大学脑与心理科学研究院, 成都 610066;2.深圳大学心理学院, 深圳 518060 |
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| 基金项目： | 国家自然科学基金面上项目(32271142 、31871130)、广东省“脑科学与类脑研究”重大科技专项: 自闭症诊疗方法研究(2018B030335001); 教育部哲学社会科学研究重大课题攻关项目(21JZD063); 深圳科学与技术研究项目(JCYJ20200109144801736)资助 |
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| 摘 要： | 睡眠问题可能会诱发恐惧相关情绪障碍(焦虑、创伤性应激障碍、恐怖症等),研究睡眠影响恐惧学习的认知神经机制,有助于增强对恐惧相关情绪障碍的预测、诊断和治疗。以往研究表明睡眠剥夺影响恐惧习得和消退主要是通过抑制vmPFC活动,阻碍其与杏仁核的功能连接,从而导致恐惧习得增强或是消退学习受损。进一步研究发现睡眠不同阶段对恐惧学习相关脑区有独特的影响:剥夺(缺乏)快速眼动睡眠会抑制vmPFC活动、增强杏仁核、海马激活,导致恐惧习得增强,消退学习受损,此外边缘皮层的功能连接减少破坏了记忆巩固(恐惧记忆和消退记忆);而慢波睡眠主要与海马变化有关,慢波睡眠期间进行目标记忆重激活可促进恐惧消退学习。未来研究需要增加睡眠影响恐惧泛化的神经机制研究、及昼夜节律中断对恐惧消退的影响,以及关注动物睡眠研究向人类睡眠研究转化中存在的问题。
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| 关 键 词： | 恐惧习得 恐惧泛化 恐惧消退 快速眼动睡眠 慢波睡眠 睡眠剥夺 睡眠障碍 |
| 收稿时间： | 2021-05-20 |
The effect of sleep on fear learning and its cognitive neural mechanisms |
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| ZHANG Jie,ZHANG Huoyin,LI Hong,LEI Yi. The effect of sleep on fear learning and its cognitive neural mechanisms[J]. Advances In Psychological Science, 2023, 31(4): 631-640. DOI: 10.3724/SP.J.1042.2023.00631 |
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| Authors: | ZHANG Jie ZHANG Huoyin LI Hong LEI Yi |
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| Affiliation: | 1.Institute of Brain and Psychological Sciences, Sichuan Normal University, Chengdu 610066, China;2.School of Psychology, Shenzhen University, Shenzhen 518060, China |
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| Abstract: | Sleep problems may induce fear-related mood disorders such as anxiety, post-traumatic stress disorder (PTSD), and phobias, among others. Studying the cognitive cognitive and neural mechanisms involved in the relationship between sleep problems and fear learning can help enhance the prediction, diagnosis, and treatment of fear-related mood disorders. Previous studies have shown that sleep deprivation affects fear acquisition mainly by inhibiting the activity of the ventral medial prefrontal cortex (vmPFC) and blocking its functional connections with the amygdala, resulting in impaired safe learning that fails to inhibit fear of threatening stimuli, thus enhancing fear acquisition. In contrast, sleep deprivation during the fear memory consolidation phase impairs the activity of the amygdala and hippocampus, thereby impairing fear memory. On the other hand, sleep deprivation during the extinction learning phase results in delayed activation of brain regions associated with extinction learning, which in turn impairs fear extinction memory. Further studies have reported that different stages of sleep have distinct effects on brain regions associated with fear learning; in particular, rapid eye movement (REM) sleep deprivation (insufficient) and complete sleep deprivation have similar effects on the cognitive and neural mechanisms of fear learning. Deprivation of REM sleep suppresses vmPFC activity, enhances amygdala activation, and thus enhances fear acquisition. In addition, reduced functional connectivity in the limbic cortex disrupts fear memory consolidation. Deprivation of REM sleep after extinction learning phase increases amygdala, insula, and dorsal anterior cingulate cortex (dACC) activity and diminishes mPFC, thereby impairing extinction memory. Therefore, after clinical treatment, quality of sleep, particularly REM sleep, should be ensured at night. In addition to reinforcing recently acquired memories, REM sleep is involved in integrating new information into existing knowledge structures, reorganizing these structures, and generalizing recently acquired memories; therefore, improving REM sleep can promote fading retention and generalization. In contrast, the slow-wave sleep (SWS) stage facilitates fear extinction learning through target memory reactivation, which allows the hippocampus to re-code threatening stimuli and accelerate the consolidation of new safety information in the amygdala. During the SWS stage, participants are not conscious and therefore do not have to directly face the threatening stimulus, thus avoiding some of the drawbacks of traditional extinction therapy applied during wakefulness for patients with fear-related mood disorders, such as anxiety disorders and (PTSD). Clinically relevant studies have found that individuals with insomnia also exhibit delayed activation of the fear extinction brain regions, with related activation occurring only during extinction recall. At the same time, individuals with insomnia have stronger learned fear which causes their insomnia and can easily develop into pathological anxiety or PTSD. Furthermore, sleep immediately following exposure therapy can optimize the therapeutic effect and may even promote extinction generalization; therefore, sleep should be used in combination with traditional exposure therapy. Future research should be conducted to further the study of the neural mechanisms by which sleep affects fear generalization and the effect of circadian rhythm disruption on fear extinction, as well as clarifying the problems in the translation of animal sleep studies to human sleep studies. |
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| Keywords: | fear acquisition fear generalization fear extinction REM SWS sleep deprivation insomnia disorder |
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