Ingiosi Ashley M, Frank Marcos G
Department of Translational Medicine and Physiology, Elson S. Floyd College of Medicine, Washington State University, Spokane, WA 99202, USA.
Gleason Institute for Neuroscience, Washington State University, Spokane, WA 99202, USA.
Clocks Sleep. 2022 Jul 7;4(3):332-345. doi: 10.3390/clockssleep4030028.
Astrocytes influence sleep expression and regulation, but the cellular signaling pathways involved in these processes are poorly defined. We proposed that astrocytes detect and integrate a neuronal signal that accumulates during wakefulness, thereby leading to increased sleep drive. Noradrenaline (NA) satisfies several criteria for a waking signal integrated by astrocytes. We therefore investigated the role of NA signaling in astrocytes in mammalian sleep. We conditionally knocked out (cKO) β2-adrenergic receptors (β2-AR) selectively in astrocytes in mice and recorded electroencephalographic and electromyographic activity under baseline conditions and in response to sleep deprivation (SDep). cKO of astroglial β2-ARs increased active phase siesta duration under baseline conditions and reduced homeostatic compensatory changes in sleep consolidation and non-rapid eye movement slow-wave activity (SWA) after SDep. Overall, astroglial NA β2-ARs influence mammalian sleep homeostasis in a manner consistent with our proposed model of neuronal-astroglial interactions.
星形胶质细胞影响睡眠的表现和调节，但参与这些过程的细胞信号通路尚不清楚。我们提出，星形胶质细胞检测并整合清醒期间积累的神经元信号，从而导致睡眠驱动力增加。去甲肾上腺素（NA）满足作为由星形胶质细胞整合的清醒信号的几个标准。因此，我们研究了NA信号在哺乳动物睡眠中的星形胶质细胞中的作用。我们有条件地在小鼠星形胶质细胞中选择性敲除（cKO）β2-肾上腺素能受体（β2-AR），并在基线条件下以及对睡眠剥夺（SDep）的反应中记录脑电图和肌电图活动。星形胶质细胞β2-AR的cKO在基线条件下增加了活跃期午睡持续时间，并减少了睡眠剥夺后睡眠巩固和非快速眼动慢波活动（SWA）中的稳态补偿变化。总体而言，星形胶质细胞NA β2-AR以与我们提出的神经元-星形胶质细胞相互作用模型一致的方式影响哺乳动物睡眠稳态。
