Resistance to extinction is associated with impaired immediate early gene induction in medial prefrontal cortex and amygdala
Resistance to extinction is associated with impaired immediate early gene induction in medial prefrontal cortex and amygdala
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DOI：
10.1111/j.1460-9568.2004.03542.x
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发表时间：
2004-08-01
影响因子：
3.4
通讯作者：
Mons, N
中科院分区：
文献类型：
--
作者：
Herry, C;Mons, N
经典恐惧条件反射的消失被认为涉及内侧前额叶皮层（mPFC）突触传递的活动依赖性增强，导致杏仁核依赖性恐惧反应的抑制。虽然许多研究已经解决了灭绝学习的潜在机制，但目前还不清楚是什么决定了灭绝记忆是否巩固或恐惧反应是否自发恢复。在这里，我们表明，使用相结合的电生理和免疫细胞化学方法，在小鼠中的条件性恐惧的自发恢复与mPFC中的突触传递的长期抑制的长期表达和mPFC和杏仁核的基底外侧核中的立即早期基因c-Fos和zif 268的诱导失败有关。这表明mPFC和杏仁核中基因表达的协调活动依赖性变化可能是长期恐惧消退记忆形成的基础。
Extinction of classical fear conditioning is thought to involve activity-dependent potentiation of synaptic transmission in the medial prefrontal cortex (mPFC), resulting in the inhibition of amygdala-dependent fear responses. While many studies have addressed the mechanisms underlying extinction learning, it is unclear what determines whether extinction memory is consolidated or whether spontaneous recovery of the fear response occurs. Here we show, using a combined electrophysiological and immunocytochemical approach, that spontaneous recovery of conditioned fear in mice is associated with a prolonged expression of long-term depression of synaptic transmission in the mPFC and the failure of induction of the immediate-early genes c-Fos and zif268 in the mPFC and the basolateral nucleus of the amygdala. This suggests that coordinated activity-dependent changes in gene expression in the mPFC and the amygdala may underlie the formation of long-term fear extinction memory.