Corcoran Kevin A, Quirk Gregory J
Department of Psychiatry, University of Puerto Rico School of Medicine, San Juan, PR, USA.
CNS Spectr. 2007 Mar;12(3):200-6. doi: 10.1017/s1092852900020915.
Anxiety disorders are commonly treated with exposure-based therapies that rely on extinction of conditioned fear. Persistent fear and anxiety following exposure therapy could reflect a deficit in the recall of extinction learning. Animal models of fear learning have elucidated a neural circuit for extinction learning and recall that includes the amygdala, ventromedial prefrontal cortex (vmPFC), and hippocampus. Whereas the amygdala is important for extinction learning, the vmPFC is a site of neural plasticity that allows for the inhibition of fear during extinction recall. We suggest that the vmPFC receives convergent information from other brain regions, such as contextual information from the hippocampus, to determine the circumstances under which extinction or fear will be recalled. Imaging studies of human fear conditioning and extinction lend credence to this extinction network. Understanding the neural circuitry underlying extinction recall will lead to more effective therapies for disorders of fear and anxiety.
焦虑症通常采用基于暴露的疗法进行治疗,这些疗法依赖于条件性恐惧的消退。暴露疗法后持续存在的恐惧和焦虑可能反映出消退学习回忆方面的缺陷。恐惧学习的动物模型已经阐明了一个用于消退学习和回忆的神经回路,其中包括杏仁核、腹内侧前额叶皮层(vmPFC)和海马体。虽然杏仁核对消退学习很重要,但vmPFC是神经可塑性的位点,它允许在消退回忆期间抑制恐惧。我们认为,vmPFC从其他脑区接收汇聚信息,例如来自海马体的情境信息,以确定回忆消退或恐惧的情况。人类恐惧条件作用和消退的影像学研究为这个消退网络提供了支持。了解消退回忆背后的神经回路将有助于开发出针对恐惧和焦虑症更有效的疗法。