Lesions of the basal amygdala block expression of conditioned fear but not extinction
Lesions of the basal amygdala block expression of conditioned fear but not extinction
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DOI：
10.1523/jneurosci.2600-05.2005
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发表时间：
2005-10-19
影响因子：
5.3
通讯作者：
Quirk, GJ
中科院分区：
文献类型：
--
作者：
Anglada-Figueroa, D;Quirk, GJ
虽然杏仁核在获得条件性恐惧中的作用已经得到了很好的证实，但关于杏仁核内回路的作用还存在争议。杏仁核外侧核（LA）被认为是恐惧条件反射可塑性的重要部位。左心房有直接和间接（通过基底核;基底杏仁核（BA））到杏仁核中央核（Ce）的投射，这是恐惧行为的基本输出。病变的LA或Ce防止收购条件冻结的条件刺激，但BA病变不，这表明BA通常不参与恐惧条件反射。如果是真的，训练后BA损伤也应该没有影响。重复之前的研究，我们发现训练前接受电解BA损伤的大鼠正常获得条件性恐惧。他们还表现出正常的长期保留和消除条件性恐惧。出乎意料的是，训练后造成的BA损伤完全阻断了条件性恐惧的表达。尽管有这种缺陷，受损的大鼠能够学习一种新的音调-电击关联。因此，虽然LA-Ce系统是足够的恐惧收购的情况下的BA，它是不够的，当BA存在，这表明BA是一个重要的网站的可塑性在恐惧条件反射。我们观察到的损伤缺陷的模式（训练后而不是训练前）可能是由稳态机制来解释的，该机制在多个输入上平衡可塑性，调节BA和LA对Ce输出神经元的影响。
Although the role of the amygdala in acquisition of conditioned fear is well established, there is debate concerning the intra-amygdala circuits involved. The lateral nucleus of the amygdala (LA) is thought to be an essential site of plasticity in fear conditioning. The LA has both direct and indirect [via the basal nuclei; basal amygdala (BA)] projections to the central nucleus (Ce) of the amygdala, an essential output for fear behaviors. Lesions of the LA or Ce prevent acquisition of conditioned freezing to a conditioned stimulus, but BA lesions do not, suggesting that the BA is not normally involved in fear conditioning. If true, posttraining BA lesions should also have no effect. Replicating previous studies, we found that rats given electrolytic BA lesions before training acquired conditioned fear normally. They also showed normal long-term retention and extinction of conditioned fear. Unexpectedly, BA lesions made after training completely blocked expression of conditioned fear. Despite this deficit, lesioned rats were able to learn a new tone-shock association. Thus, although the LA-Ce system is sufficient for fear acquisition in the absence of the BA, it is not sufficient when the BA is present, suggesting that the BA is an important site of plasticity in fear conditioning. The pattern of lesion deficits we observed (after but not before training) might be explained by homeostatic mechanisms that balance plasticity over multiple inputs, regulating the influence of the BA and LA onto Ce output neurons.