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Selective neuronal lapses precede human cognitive lapses following sleep deprivation.
Nature Medicine ( IF 58.7 ) Pub Date : 2017-Dec-01 , DOI: 10.1038/nm.4433
Yuval Nir , Thomas Andrillon , Amit Marmelshtein , Nanthia Suthana , Chiara Cirelli , Giulio Tononi , Itzhak Fried

Sleep deprivation is a major source of morbidity with widespread health effects, including increased risk of hypertension, diabetes, obesity, heart attack, and stroke. Moreover, sleep deprivation brings about vehicle accidents and medical errors and is therefore an urgent topic of investigation. During sleep deprivation, homeostatic and circadian processes interact to build up sleep pressure, which results in slow behavioral performance (cognitive lapses) typically attributed to attentional thalamic and frontoparietal circuits, but the underlying mechanisms remain unclear. Recently, through study of electroencephalograms (EEGs) in humans and local field potentials (LFPs) in nonhuman primates and rodents it was found that, during sleep deprivation, regional 'sleep-like' slow and theta (slow/theta) waves co-occur with impaired behavioral performance during wakefulness. Here we used intracranial electrodes to record single-neuron activities and LFPs in human neurosurgical patients performing a face/nonface categorization psychomotor vigilance task (PVT) over multiple experimental sessions, including a session after full-night sleep deprivation. We find that, just before cognitive lapses, the selective spiking responses of individual neurons in the medial temporal lobe (MTL) are attenuated, delayed, and lengthened. These 'neuronal lapses' are evident on a trial-by-trial basis when comparing the slowest behavioral PVT reaction times to the fastest. Furthermore, during cognitive lapses, LFPs exhibit a relative local increase in slow/theta activity that is correlated with degraded single-neuron responses and with baseline theta activity. Our results show that cognitive lapses involve local state-dependent changes in neuronal activity already present in the MTL.

中文翻译:

睡眠剥夺后,选择性神经元失误先于人类认知失误。

睡眠剥夺是发病率的主要来源,具有广泛的健康影响,包括增加患高血压,糖尿病,肥胖,心脏病和中风的风险。此外,睡眠不足会导致交通事故和医疗事故,因此是研究的紧迫课题。在睡眠剥夺期间,体内稳态和昼夜节律过程相互作用以建立睡眠压力,这导致通常归因于注意丘脑和额顶回路的行为表现减慢(认知障碍),但其潜在机制尚不清楚。最近,通过研究人类的脑电图(EEG)和非人类的灵长类动物和啮齿动物的局部场电势(LFP),我们发现在睡眠剥夺期间,区域性的“类似睡眠” 在清醒时,慢波和θ(慢/θ)波会与行为表现受损并存。在这里,我们使用颅内电极记录人类神经外科患者在多个实验阶段(包括整夜睡眠剥夺后的一个阶段)执行面部/非面部分类心理运动警戒任务(PVT)的单神经元活动和LFP。我们发现,就在认知丧失之前,内侧颞叶(MTL)中单个神经元的选择性尖峰反应被减弱,延迟和延长。当比较最慢的行为PVT反应时间与最快的行为时间时,这些“神经元失误”在逐项试验中是显而易见的。此外,在认知失误期间,LFPs表现出慢/θ活性的相对局部增加,这与降解的单神经元反应和基线theta活性相关。我们的结果表明,认知障碍涉及MTL中已经存在的神经元活动的局部状态依赖性变化。
更新日期:2017-11-06
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