Norwegian Centre for Mental Disorders Research (NORMENT), KG Jebsen Centre for Psychosis Research, Oslo University Hospital, Norway; Department of Neurology, Oslo University Hospital, Norway; Institute of Clinical Medicine, University of Oslo, Norway.
Cognitive Neurology Research Unit, Sunnybrook Health Sciences Centre, Toronto, Canada; Department of Radiology, Amsterdam University Medical Center, the Netherlands.
Neuroimage. 2019 Feb 1;186:497-509. doi: 10.1016/j.neuroimage.2018.11.032. Epub 2018 Nov 22.
Elucidating the neurobiological effects of sleep and wake is an important goal of the neurosciences. Whether and how human cerebral blood flow (CBF) changes during the sleep-wake cycle remain to be clarified. Based on the synaptic homeostasis hypothesis of sleep and wake, we hypothesized that a day of wake and a night of sleep deprivation would be associated with gray matter resting CBF (rCBF) increases and that sleep would be associated with rCBF decreases. Thirty-eight healthy adult males (age 22.1 ± 2.5 years) underwent arterial spin labeling perfusion magnetic resonance imaging at three time points: in the morning after a regular night's sleep, the evening of the same day, and the next morning, either after total sleep deprivation (n = 19) or a night of sleep (n = 19). All analyses were adjusted for hematocrit and head motion. rCBF increased from morning to evening and decreased after a night of sleep. These effects were most prominent in bilateral hippocampus, amygdala, thalamus, and in the occipital and sensorimotor cortices. Group × time interaction analyses for evening versus next morning revealed significant interaction in bilateral lateral and medial occipital cortices and in bilateral insula, driven by rCBF increases in the sleep deprived individuals and decreases in the sleepers, respectively. Furthermore, group × time interaction analyses for first morning versus next morning showed significant effects in medial and lateral occipital cortices, in anterior cingulate gyrus, and in the insula, in both hemispheres. These effects were mainly driven by CBF increases from TP1 to TP3 in the sleep deprived individuals. There were no associations between the rCBF changes and sleep characteristics, vigilant attention, or subjective sleepiness that remained significant after adjustments for multiple analyses. Altogether, these results encourage future studies to clarify mechanisms underlying sleep-related rCBF changes.
阐明睡眠和觉醒的神经生物学效应是神经科学的一个重要目标。人类大脑血液流量(CBF)在睡眠-觉醒周期中是否以及如何变化仍有待阐明。基于睡眠和觉醒的突触稳态假说,我们假设一天的觉醒和一夜的睡眠剥夺将与灰质静息 CBF(rCBF)增加有关,而睡眠将与 rCBF 减少有关。38 名健康成年男性(年龄 22.1±2.5 岁)在三个时间点接受动脉自旋标记灌注磁共振成像:正常睡眠后的早晨、同一天的傍晚和第二天的早晨,要么是在完全睡眠剥夺后(n=19),要么是在一夜睡眠后(n=19)。所有分析均根据红细胞压积和头部运动进行调整。rCBF 从早晨到傍晚增加,一夜睡眠后减少。这些影响在双侧海马体、杏仁核、丘脑以及枕叶和感觉运动皮层最为明显。傍晚与第二天早晨的组×时间交互分析显示,在双侧外侧和内侧枕叶以及双侧岛叶存在显著的交互作用,这是由睡眠剥夺者的 rCBF 增加和睡眠者的 rCBF 减少驱动的。此外,第一次早晨与第二天早晨的组×时间交互分析显示,在双侧枕叶和外侧枕叶、前扣带回和岛叶,以及双侧都有显著的影响。这些影响主要是由睡眠剥夺者从 TP1 到 TP3 的 CBF 增加驱动的。在调整了多项分析后,rCBF 变化与睡眠特征、警觉注意力或主观困倦之间没有关联。总的来说,这些结果鼓励未来的研究阐明与睡眠相关的 rCBF 变化的机制。