导读 | 除了酒驾,不少交通事故都与司机疲劳驾驶有关。为什么会发生这些意外呢?科学家们发现,睡眠不足,会影响大脑细胞之间的交流,最终导致记忆、视觉感知暂时性地“走神”。 |
之前的研究已经表明,睡眠不足与抑郁、肥胖、糖尿病、心脏病、中风等风险有关。现在,这一发表在《Nature Medicine》上的研究再次“重申”睡眠的重要性——来自于加州大学的研究团队从更深层面解析了睡眠不足对大脑的影响,发现缺觉会剥夺神经元正常工作的能力。
睡眠不足干扰大脑工作效率
加州大学洛杉矶分校David Geffen 医学院的神经外科教授Itzhak Fried带领团队研究了12名癫痫患者(大脑都植入电极,以便记录手术前癫痫发作的大脑区域)。考虑到睡眠不足会引发癫痫发作,这些受试者被要求整夜不睡,以加速癫痫发作,缩短住院时间。
同时,患者需要完成相关任务——对各种图像进行分类。研究人员会通过电极实时记录近1500个脑细胞的活动情况,其中主要关注掌控视觉感知、记忆的颞叶区域。
结果发现,当患者越来越困倦时,他们执行图像分类任务会变得越来越困难。当身体速度放缓时,他们的大脑运作也会减慢。
睡眠不足干扰大脑细胞正常交流(视频来源:UCLA)
视频腾讯地址:https://v.qq.com/x/page/l0501lxnc9s.html
睡眠不足类似于喝醉酒
“我们着迷于观察睡眠不足对大脑活动的消极作用。” 文章作者、特拉维夫大学的Yuval Nir博士表示,“不同于平常的快速反应,困倦情况下的神经元反应速度减慢、信号减弱、神经递质的运输时间延长。”
缺少睡眠会干扰神经元编码、处理信息,包括视觉。所以,会有睡眠不足的司机在突发路况下反应不及时。“司机疲惫不堪的大脑会减缓反应的速度,需要更长的时间处理感知到的事物,从而埋下事故的隐患。” Itzhak Fried解释道。
研究团队发现,在12名患者大脑的同一区域,大脑细胞活跃度下降。这意味着,大脑的一些特定区域会因为缺觉而神经衰退。而其他的大脑区域会像往常一样清醒着运作。
“睡眠不足对大脑的影响,类似于喝醉酒。”Itzhak Fried表示,“但是不同于酒驾检测,目前还没有法律或者医疗标准鉴定疲劳驾驶的司机。”
编者后记
除了干扰脑细胞交流,睡眠障碍还是阿尔兹海默症认知功能降低的典型特征之一,而且是预测未来发生阿尔兹海默症风险的重要因素。
已有研究团队证实,睡眠不足会造成淀粉样蛋白在大脑中聚集,影响产生深度睡眠的脑区。这一后果会进一步阻止夜间大脑对淀粉样蛋白的清除工作,从而进入一个恶性循环——淀粉样蛋白越积越多,睡眠越来越少。而且,长期的睡眠不足,会导致大脑进入过度负载状态,从而开始摧毁受损的细胞,埋下神经类疾病的祸端。
所以,我们需要善待自己,先保证一个充足的睡眠,用它调整好生活的呼吸!
参考资料:
New study reveals sleep deprivation disrupts brain-cell communication
Sleep deprivation is a major source of morbidity with widespread health effects, including increased risk of hypertension, diabetes, obesity, heart attack, and stroke1. Moreover, sleep deprivation brings about vehicle accidents and medical errors2, 3, 4 and is therefore an urgent topic of investigation. During sleep deprivation, homeostatic and circadian processes interact to build up sleep pressure5, which results in slow behavioral performance (cognitive lapses) typically attributed to attentional thalamic and frontoparietal circuits6, 7, 8, 9, 10, 11, 12, 13, 14, but the underlying mechanisms remain unclear3, 15. Recently, through study of electroencephalograms (EEGs) in humans16, 17 and local field potentials (LFPs) in nonhuman primates18 and rodents19 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)20, 21, 22, 23, 24 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.
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