Anxiety, sleep disruption and emotional brain dysregulation

描述（由申请人提供）：睡眠中断是焦虑症谱系中公认的问题症状。患有焦虑症的个体还表现出杏仁核对厌恶刺激的反应增强的标志性特征。独立地，健康参与者的睡眠不足导致杏仁核反应放大，以及焦虑水平升高，而睡眠的有益存在相反地提供了第二天厌恶反应和焦虑的姑息性减少。尽管有这些平行的证据，睡眠，焦虑和情绪大脑反应之间的关系仍然没有特征。探索这种潜在的因果关系的必要性不仅是为了更深入地了解焦虑的病理生理病因学，而且也是为了改善焦虑的预防策略和有效治疗的发展。通过结合功能性磁共振成像（fMRI）、睡眠脑电图记录和神经行为评估的单独实验，该提案将检验以下假设：高度焦虑状态（1）阻止睡眠在调节第二天杏仁核反应性方面的正常生理益处，（2）使杏仁核更容易受到睡眠不足的加重影响，以及（3）否定了睡眠丧失后恢复睡眠在恢复正常杏仁核反应性方面的益处。因此，该建议代表了对焦虑状态如何改变最佳情绪大脑功能的睡眠依赖性调节以及睡眠不足如何有助于与高焦虑状态相关的放大神经信号的系统评估。了解焦虑，睡眠障碍和情绪脑反应之间的因果关系具有相当大的临床和公共卫生影响，以及直接转化治疗的适用性。此外，考虑到整个社会的睡眠时间持续减少，特别是在易受焦虑相关情绪困难影响的年轻人群中，这些研究的适用性进一步增加。

DESCRIPTION (provided by applicant): Sleep disruption is a recognized and problematic symptom across the anxiety disorders spectrum. Individuals suffering anxiety additionally display a hallmark signature of enhanced amygdala reactivity to aversive stimuli. Independently, sleep loss in healthy participants results in amplified amygdala reactivity, together with raised levels of anxiety, while the beneficial presence of sleep conversely offers a palliative reduction in next-day aversive reactivity and anxiety. Despite these parallel lines of evidence, the relationship between sleep, anxiety and emotional brain reactivity remains uncharacterized. The need to explore this potentially causal interaction is not only imperative for gaining a deeper understanding of the pathophysiological etiology underlying anxiety, but also for the development of improved preventative strategies and effective treatments for amelioration of anxiety. Across separate experiments combining functional MRI (fMRI), sleep EEG recordings and neurobehavioral assessments, this proposal will test the hypothesis that high anxiety status (1) prevents the normal physiological benefit of sleep in regulating next-day amygdala reactivity, (2) imposes greater vulnerability of the amygdala to the aggravating effects of sleep loss, and (3) negates the benefit of recovery sleep in restoring normative amygdala reactivity, following sleep loss. As such, this proposal represents a systematic evaluation of how anxiety status alters the sleep-dependent regulation of optimal emotional brain function, and how a lack of sleep contributes to the amplified neural signature associated with high anxiety status. Understanding the causal associations between anxiety, sleep impairment, and emotional brain reactivity has considerable clinical and public health ramifications, as well as direct translational treatment applicability. Moreover, considering the continued erosion of sleep time across society, particularly in young populations susceptible to anxiety-related emotion difficulties, the applicability of these studies further increases in relevance.