The synaptic networks in the amygdala have been the subject of intense interest in recent times, primarily because of the role of this structure in emotion. Fear and its extinction depend on the workings of these networks, with particular interest in extinction because of its potential to ameliorate adverse symptoms associated with post-traumatic stress disorder. Here we place emphasis on the extinction networks revealed by recent techniques, and on the probable plasticity properties of their synaptic connections. We use modules of neurons representing each of the principal components identified as involved in extinction. Each of these modules consists of neural networks, containing specific ratios of excitatory and specialized inhibitory neurons as well as synaptic plasticity mechanisms appropriate for the component of the amygdala they represent. While these models can produce dynamic output, here we concentrate on the equilibrium outputs and do not model the details of the plasticity mechanisms. Pavlovian fear conditioning generates a fear memory in the lateral amygdala module that leads to activation of neurons in the basal nucleus fear module but not in the basal nucleus extinction module. Extinction protocols excite infralimbic medial prefrontal cortex neurons (IL) which in turn excite so-called extinction neurons in the amygdala, leading to the release of endocannabinoids from them and an increase in efficacy of synapses formed by lateral amygdala neurons on them. The model simulations show how such a mechanism could explain experimental observations involving the role of IL as well as endocannabinoids in different temporal phases of extinction.

近年来，杏仁核中的突触网络引起了人们极大的兴趣，这主要是由于这种结构在情感中的作用。恐惧及其灭绝取决于这些网络的运作，对灭绝特别感兴趣，因为它有可能缓解与创伤后应激障碍相关的不良症状。在这里，我们将重点放在由最新技术揭示的灭绝网络上，并强调其突触连接的可能可塑性。我们使用神经元模块来表示被确定为灭绝的每个主要成分。这些模块中的每个模块都由神经网络组成，其中包含特定比例的兴奋性和专门抑制性神经元，以及适合于它们所代表的杏仁核成分的突触可塑性机制。尽管这些模型可以产生动态输出，但在这里我们只关注平衡输出，而没有对可塑性机制的细节进行建模。巴甫洛夫式恐惧调节在外侧杏仁核模块中产生恐惧记忆，从而导致基底核恐惧模块中神经元的激活，而不是基底核消失模块中的神经元的激活。灭绝方案激发下肢内侧前额叶皮层神经元（IL），继而又激发杏仁核中的所谓灭绝神经元，从而导致它们释放内源性大麻素，并增加外侧杏仁核神经元在其上形成的突触的功效。模型仿真表明，这种机制如何解释实验观察，涉及IL和内源性大麻素在不同灭绝时间阶段的作用。