觉醒激活的神经元群体调控睡眠驱动
觉醒激活的神经元群体调控睡眠驱动
作者： 小柯机器人 发布时间：2026/8/20 17:05:25
本期文章：《自然》：Online/在线发表
瑞士巴塞尔大学Clare Diester等合作 发现了调控睡眠驱动的觉醒激活神经元群体。 相关论文于2026年8月19日发表于国际顶尖学术期刊《自然》杂志上。
长时间觉醒会增加睡眠驱动，通常由增加的睡眠来补偿。这种睡眠的稳态调节深刻影响着我们的生活，但其背后的神经环路机制仍知之甚少。在此，研究人员利用全脑活动图谱、靶向神经操纵和电生理技术，鉴定了小鼠中调控睡眠驱动的觉醒激活神经元。通过比较对睡眠剥夺、恢复性睡眠和昼夜节律行为的全脑反应，研究人员将前内侧视前区和中缝核确定为编码睡眠缺失的候选脑区。激活这些区域中对睡眠剥夺有反应的细胞，可诱导睡眠时长和强度的增加，类似于恢复性睡眠。相反，抑制对剥夺有反应的细胞则会减少睡眠，并消除通常在剥夺期间观察到的睡眠倾向增加。中缝核中对睡眠剥夺有反应的神经元投射至皮层下睡眠相关脑区，并通过视前下丘脑发挥作用。这些对剥夺敏感的细胞包括血清素能神经元和一群独特的GABA能神经元，后者在睡眠剥夺期间内在兴奋性增加。GABA能神经元与血清素能神经元的共激活协同促进睡眠，而共抑制则使睡眠慢性减少近70%。值得注意的是，尽管睡眠显著减少，大多数小鼠仍存活，且未出现睡眠驱动的补偿性增加，也未出现通常与严重睡眠剥夺相关的行为缺陷。总之，这些结果定义了在觉醒期间被激活且对睡眠驱动至关重要的神经元群体。
附：英文原文
Title: Wake-activated neuronal populations that regulate sleep drive
Author: Joo, William, Diester, Clare, Bitsikas, Vassilis, Panopoulou, Myrto, Hidalgo, Amelia, Ntemos, Konstantinos, Pena, Rodrigo C. G., Imhof, Fabia, Odstrcil, Iris, Donato, Flavio, Fucile, Geoffrey, Kroeger, Daniel, Scammell, Thomas E., Schier, Alexander F.
Issue&Volume: 2026-08-19
Abstract: Prolonged wakefulness increases sleep drive and is normally compensated for by increased sleep1,2,3. This homeostatic regulation of sleep shapes our lives profoundly, but the underlying neural circuit mechanisms remain poorly understood. Here, we identify wake-activated neurons that regulate sleep drive in mice, using whole-brain activity mapping, targeted neuronal manipulations and electrophysiology. By comparing whole-brain responses to sleep deprivation, recovery sleep and circadian behaviour, we identify the anterior medial preoptic area and the median raphe as candidate regions that encode sleep deficit. Activating sleep-deprivation-responsive cells in these regions induces increases in sleep duration and intensity that resemble recovery sleep. Conversely, inhibiting deprivation-responsive cells reduces sleep and abolishes the increased sleep propensity usually observed during deprivation. Neurons in the median raphe that are responsive to sleep deprivation project to subcortical sleep-associated regions and act through the preoptic hypothalamus. These deprivation-sensitive cells include serotonergic neurons and a distinct population of GABAergic neurons, whose intrinsic excitability increases during sleep deprivation. Co-activation of GABAergic and serotonergic neurons synergistically promotes sleep, whereas co-inhibition chronically decreases sleep by nearly 70%. Remarkably, most mice survive despite this marked reduction in sleep, without the compensatory increases in sleep drive or the behavioural deficits typically associated with severe sleep deprivation. Together, these results define neuronal populations that are activated during wakefulness and are crucial for sleep drive.
DOI: 10.1038/s41586-026-10928-3
Source: https://www.nature.com/articles/s41586-026-10928-3