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Imbalance of approach and avoidance: the yin and yang of anxiety disorders.

机译:进近和回避的不平衡:焦虑症的阴阳。

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Two interesting articles from Harvard University investigators in this issue of Biological Psychiatry challenge us to reconsider and rethink the complexities of the underlying neurobiology of posttraumatic stress disorder (PTSD). We refer to these articles with a view to highlighting their unique contributions to the literature and the new directions they motivate for translational research in PTSD and other anxiety disorders. Milad and colleagues (1) used an operant conditioning paradigm to show that patients with PTSD have deficient extinction retention relative to trauma-exposed control subjects who had not developed PTSD. They further demonstrate, using functional MRI (fMRI), that this reduced extinction retention is related to less activation in the hippocampus and bilateral ventromedial prefrontal cortex in patients with PTSD. This article underscores our growing appreciation that PTSD is characterized by dysfunction of "unlearning" within fear circuitry, and the findings should motivate clinical research to enhance extinction retention through pharmacologic and other means. Such approaches, in parallel with those aimed at the disruption of the consolidation of fear memories, are among the most promising translational leads for PTSD therapeutics (2).
机译:哈佛大学研究人员在本期《生物精神病学》上发表的两篇有趣的文章向我们提出挑战,要求我们重新考虑和重新思考创伤后应激障碍(PTSD)的潜在神经生物学的复杂性。我们参考这些文章是为了突出它们对文献的独特贡献以及它们为PTSD和其他焦虑症的转化研究所激发的新方向。 Milad及其同事(1)使用操作性条件范式来证明PTSD患者相对于未患PTSD的暴露于创伤的对照对象而言,其retention灭保持力不足。他们进一步使用功能性MRI(fMRI)证明,这种减少的绝灭保留与PTSD患者海马和双侧腹膜前额叶皮层的激活减少有关。本文强调了我们日益认识到,PTSD的特征是恐惧回路中“无法学习”的功能障碍,这些发现应能激发临床研究,以通过药理学和其他手段来增强灭绝效果。此类方法与旨在破坏恐惧记忆巩固的方法相平行,是PTSD治疗药物最有希望的翻译线索之一(2)。

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