Alterations in microglial morphology concentrate in the habitual sleeping period of the mouse.

In nocturnal animals, waking appears during the dark period while maximal non-rapid-eye-movement sleep (NREMS) with electroencephalographic slow-wave-activity (SWA) takes place at the beginning of the light period. Vigilance states associate with variable levels of neuronal activity: waking with high-frequency activity patterns while during NREMS, SWA influences neuronal activity in many brain areas. On a glial level, sleep deprivation modifies microglial morphology, but only few studies have investigated microglia through the physiological sleep-wake cycle.

Roles of Microglial Phagocytosis and Inflammatory Mediators in the Pathophysiology of Sleep Disorders.

Sleep serves crucial learning and memory functions in both nervous and immune systems. Microglia are brain immune cells that actively maintain health through their crucial physiological roles exerted across the lifespan, including phagocytosis of cellular debris and orchestration of neuroinflammation. The past decade has witnessed an explosive growth of microglial research.

Inducible nitric oxide synthase and AMP-activated protein kinase in basal forebrain during prolonged waking.

Activation of inducible nitric oxide synthase (iNOS) and the subsequent production of adenosine in basal forebrain in the early phase of prolonged waking suggest that the wake-promoting basal forebrain is selectively sensitive to the metabolic demands of waking. In this study, iNOS protein, and activation of AMP-activated protein kinase - a marker of decreased cellular energy charge - were measured in the rat basal forebrain and cortex during prolonged waking (1.5-, 3- and 6 h).