Sleep is a natural occurring state of decreased arousal that is crucial for normal cardiovascular, immune and cognitive function (Rosenberg-Adamsen et al., 1996; Saper et al., 2010). However, the principal sedative drugs, most of which modulate the γ amino butyric acid A (GABAA) receptor, do not produce the neurophysiological oscillations of sleep (Akeju et al., 2017). Rather, they produce neurophysiological oscillations that reflect cortical circuit disruptions, which manifest as electroencephalogram frontal beta oscillations, frontal alpha oscillations, burst suppression and isoelectricity (Patat et al., 1994; Feinberg et al., 2000; van Lier et al., 2004; Purdon et al., 2013; Akeju et al., 2014a; Akeju et al., 2014b, Akeju et al., 2017).
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Παρασκευή 20 Οκτωβρίου 2017
Dexmedetomidine promotes biomimetic non-rapid eye movement stage 3 sleep in humans: A pilot study
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