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利用条件性恐惧应激(CFS)动物模型来理解焦虑的神经生物学机制和药物治疗。

Using the conditioned fear stress (CFS) animal model to understand the neurobiological mechanisms and pharmacological treatment of anxiety.

作者信息

Li Xiaobai

机构信息

Department of Psychiatry, the First Hospital of China Medical University, Shenyang, Liaoning Province, China.

出版信息

Shanghai Arch Psychiatry. 2012 Oct;24(5):241-9. doi: 10.3969/j.issn.1002-0829.2012.05.001.

Abstract

The mechanisms underlying the etiology and pathophysiology of anxiety disorders - the most prevalent class of mental disorders - remain unclear. Over the last 30 years investigators have used the animal model of conditioned fear stress (CFS) to investigate the brain structures and neurotransmitter systems involved in aversive emotional learning and memory. Recent studies have focused on the neuronal circuitry and cellular mechanisms of fearful emotional experiences. This review describes the CFS paradigm, discusses the neural circuit and neurotransmission underlying CFS, and explains the mechanism of action of pharmacological treatments of CFS. The focus of the review is on the molecular mechanisms of fear extinction, a phenomenon directly implicated in the clinical treatment of anxiety. Based on our assessment of previous work we will conclude by considering potential molecular targets for treating symptoms of anxiety and fear.

摘要

焦虑症是最常见的一类精神障碍,其病因和病理生理学背后的机制仍不清楚。在过去30年里,研究人员利用条件性恐惧应激(CFS)动物模型来研究参与厌恶情绪学习和记忆的脑结构和神经递质系统。最近的研究集中在恐惧情绪体验的神经回路和细胞机制上。本综述描述了CFS范式,讨论了CFS背后的神经回路和神经传递,并解释了CFS药物治疗的作用机制。综述的重点是恐惧消退的分子机制,这一现象与焦虑症的临床治疗直接相关。基于我们对以往工作的评估,我们将通过考虑治疗焦虑和恐惧症状的潜在分子靶点来得出结论。

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