Clinical Neuroscience Division, School of Medicine, University of Southampton, Southampton, UK.
Neuropsychopharmacology. 2011 Jul;36(8):1557-62. doi: 10.1038/npp.2011.15. Epub 2011 Apr 13.
Inhalation of 7.5% CO(2) increases anxiety and autonomic arousal in humans, and elicits fear behavior in animals. However, it is not known whether CO(2) challenge in humans induces dysfunction in neurocognitive processes that characterize generalized anxiety, notably selective attention to environmental threat. Healthy volunteers completed an emotional antisaccade task in which they looked toward or away from (inhibited) negative and neutral stimuli during inhalation of 7.5% CO(2) and air. CO(2) inhalation increased anxiety, autonomic arousal, and erroneous eye movements toward threat on antisaccade trials. Autonomic response to CO(2) correlated with hypervigilance to threat (speed to initiate prosaccades) and reduced threat inhibition (increased orienting toward and slower orienting away from threat on antisaccade trials) independent of change in mood. Findings extend evidence that CO(2) triggers fear behavior in animals via direct innervation of a distributed fear network that mobilizes the detection of and allocation of processing resources toward environmental threat in humans.
吸入 7.5%的二氧化碳会增加人类的焦虑和自主唤醒，并在动物中引发恐惧行为。然而，目前尚不清楚二氧化碳暴露是否会导致人类神经认知过程出现功能障碍，而这些认知过程正是广泛性焦虑的特征，尤其是对环境威胁的选择性注意。健康志愿者在吸入 7.5%的二氧化碳和空气时，完成了一项情绪性反扫视任务，即在看到负性和中性刺激时，他们需要看向或不看向（抑制）这些刺激。二氧化碳吸入增加了反扫视试验中对威胁的焦虑、自主唤醒和错误眼动。对二氧化碳的自主反应与对威胁的过度警惕（启动正扫视的速度）相关，并且减少了对威胁的抑制（在反扫视试验中，对威胁的定向更快，定向离开威胁的速度更慢），而与情绪变化无关。这些发现扩展了证据，表明二氧化碳通过直接支配一个分布式恐惧网络来触发动物的恐惧行为，该网络调动了对人类环境威胁的检测和处理资源的分配。
