Plastic synaptic networks of the amygdala for the acquisition, expression, and extinction of conditioned fear.
Plastic synaptic networks of the amygdala for the acquisition, expression, and extinction of conditioned fear.
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DOI：
10.1152/physrev.00037.2009
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发表时间：
2010-04
影响因子：
33.6
通讯作者：
Pare D
中科院分区：
文献类型：
--
作者：
Pape HC;Pare D
在过去的十年里，人们对经典条件性恐惧反应的获得和消失的机制产生了浓厚的兴趣。在某种程度上，这是由于认识到恐惧学习机制的异常可能参与人类焦虑症的发展和/或维持。这种学习范式的简单性和鲁棒性，再加上底层电路在进化上很好地保守这一事实，使其成为研究记忆的基础生物学和识别调节学习恐惧的正常和病理表达的遗传因素和神经元系统的理想模型。在确定恐惧获得后的神经元功能如何在恐惧记忆巩固过程中变得稳定以及这些过程如何在恐惧记忆消退过程中受到控制方面取得了重大进展。随着这些进展，人们认识到，远程神经元网络中的活动必须协调这些事件的发生。在本文中，我们回顾了这些协调网络活动的机制和分子级联导致持久的恐惧记忆，并允许它们的灭绝。我们将把重点放在巴甫洛夫恐惧条件反射作为一个模型和杏仁核作为获得和消除恐惧反应的关键组成部分。
The last ten years have witnessed a surge of interest for the mechanisms underlying the acquisition and extinction of classically conditioned fear responses. In part, this results from the realization that abnormalities in fear learning mechanisms likely participate to the development and/or maintenance of human anxiety disorders. The simplicity and robustness of this learning paradigm, coupled to the fact that the underlying circuitry is evolutionarily well conserved makes it an ideal model to study the basic biology of memory and identify genetic factors and neuronal systems that regulate the normal and pathological expressions of learned fear. Critical advances have been made in determining how modified neuronal functions upon fear acquisition become stabilized during fear memory consolidation and how these processes are controlled in the course of fear memory extinction. With these advances, came the realization that activity in remote neuronal networks must be coordinated for these events to take place. In this paper, we review these mechanisms of coordinated network activity and the molecular cascades leading to enduring fear memory, and allowing for their extinction. We will focus on Pavlovian fear conditioning as a model and the amygdala as a key component for the acquisition and extinction of fear responses.
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