Serotonergic modulation of conditioned fear.
Serotonergic modulation of conditioned fear.
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DOI：
10.6064/2012/821549
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发表时间：
2012
期刊：
影响因子：
3.2
通讯作者：
Homberg JR
中科院分区：
文献类型：
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作者：
Homberg JR
条件恐惧在焦虑症、抑郁症和其他神经精神疾病中起着关键作用。了解神经调节剂如何驱动相关的学习和记忆过程，包括记忆巩固、检索/表达和消退（回忆），对于理解这些疾病及其治疗（易感性的个体差异）至关重要。我在这里回顾的人类和啮齿动物研究共同揭示了，除其他外，急性选择性血清素再摄取抑制剂（SSRI）治疗促进恐惧条件反射，减少情境恐惧，增加线索恐惧，慢性SSRI治疗减少情境恐惧和线索恐惧，5-HT1A受体抑制情境恐惧的获得和表达，5-HT2A受体促进线索恐惧和情境恐惧的巩固，5-HT2C受体的失活促进了线索恐惧记忆的检索，5-HT3受体介导情境恐惧，基因诱导的血清素水平增加与恐惧条件反射增加、线索恐惧消退受损或消退回忆受损有关，基因诱导的5-HT消耗增加了恐惧条件反射和情境恐惧。为了调和血清素水平和条件性恐惧之间看似矛盾的关系，提出了几种解释。
Conditioned fear plays a key role in anxiety disorders as well as depression and other neuropsychiatric conditions. Understanding how neuromodulators drive the associated learning and memory processes, including memory consolidation, retrieval/expression, and extinction (recall), is essential in the understanding of (individual differences in vulnerability to) these disorders and their treatment. The human and rodent studies I review here together reveal, amongst others, that acute selective serotonin reuptake inhibitor (SSRI) treatment facilitates fear conditioning, reduces contextual fear, and increases cued fear, chronic SSRI treatment reduces both contextual and cued fear, 5-HT1A receptors inhibit the acquisition and expression of contextual fear, 5-HT2A receptors facilitates the consolidation of cued and contextual fear, inactivation of 5-HT2C receptors facilitate the retrieval of cued fear memory, the 5-HT3 receptor mediates contextual fear, genetically induced increases in serotonin levels are associated with increased fear conditioning, impaired cued fear extinction, or impaired extinction recall, and that genetically induced 5-HT depletion increases fear conditioning and contextual fear. Several explanations are presented to reconcile seemingly paradoxical relationships between serotonin levels and conditioned fear.