The role of the medial prefrontal cortex-amygdala circuit in stress effects on the extinction of fear.

The role of the medial prefrontal cortex-amygdala circuit in stress effects on the extinction of fear.
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DOI:
10.1155/2007/30873
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发表时间:
2007
期刊:
影响因子:
3.1
通讯作者:
Maroun M
Maroun M
中科院分区:
医学4区
文献类型:
--
作者:
Akirav I;Maroun M

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压力暴露,取决于其强度和持续时间,以适应或不适应的方式影响认知和学习。关于压力对认知过程的影响的研究主要集中在条件恐惧上,因为有人认为恐惧驱动的学习是情感障碍和焦虑障碍的根源。通过实验消除对诱发恐惧刺激的恐惧反应,可以实现对恐惧动机反应的抑制。越来越多的证据表明,恐惧记忆的消失需要内侧前额叶皮层和杏仁核的可塑性。这些大脑区域也深度参与调节压力对记忆的影响。此外,大量证据表明γ -氨基丁酸(GABA)的传递在应激经历引起的行为后遗症的调节中起主要作用,也可能部分介导灭绝过程中的抑制性学习。在这篇综述中,我们提供的证据表明,暴露于压力经历可能会损害恐惧消退和GABA系统的可能参与。恐惧消退学习障碍尤其重要,因为它可能使一些人容易患上创伤后应激障碍。我们进一步讨论了内侧前额叶皮层-杏仁核回路在应激经历后可能出现的功能障碍,这可能解释了暴露于应激源导致的灭绝受损。
Stress exposure, depending on its intensity and duration, affects cognition and learning in an adaptive or maladaptive manner. Studies addressing the effects of stress on cognitive processes have mainly focused on conditioned fear, since it is suggested that fear-motivated learning lies at the root of affective and anxiety disorders. Inhibition of fear-motivated response can be accomplished by experimental extinction of the fearful response to the fear-inducing stimulus. Converging evidence indicates that extinction of fear memory requires plasticity in both the medial prefrontal cortex and the amygdala. These brain areas are also deeply involved in mediating the effects of exposure to stress on memory. Moreover, extensive evidence indicates that gamma-aminobutyric acid (GABA) transmission plays a primary role in the modulation of behavioral sequelae resulting from a stressful experience, and may also partially mediate inhibitory learning during extinction. In this review, we present evidence that exposure to a stressful experience may impair fear extinction and the possible involvement of the GABA system. Impairment of fear extinction learning is particularly important as it may predispose some individuals to the development of posttraumatic stress disorder. We further discuss a possible dysfunction in the medial prefrontal cortex-amygdala circuit following a stressful experience that may explain the impaired extinction caused by exposure to a stressor.