Disease relevance of Wakefulness

• Clinical studies have defined pathologies of wakefulness: coma, the persistent vegetative state, the 'locked-in' syndrome, akinetic mutism and brain death [1].
• During wakefulness, similar changes in ventricular extrasystoles and heart rate could be produced by the intravenous administration of propranolol and, to a lesser extent, by phenylephrine [2].
• Sleep architecture and quantitative EEG from wakefulness and REM sleep were studied in six patients (mean age, 70.5 years) with progressive supranuclear palsy (PSP) and compared with that of six control subjects (mean age, 69.8 years) [3].
• Retinal cholesterol emboli were seen in one half of the patients regardless of whether the retinal infarction had occurred during sleep or wakefulness [4].
• To define the chronobiology of glucose tolerance and insulin secretion in obesity, nine obese men and nine lean men were studied during constant glucose infusion for 53 h, including 8 h of nocturnal sleep, 28 h of continuous wakefulness, and 8 h of daytime sleep [5].

Psychiatry related information on Wakefulness

• Targeted disruption of the orexin gene in mice produces a syndrome remarkably similar to human and canine narcolepsy, a sleep disorder characterized by excessive daytime sleepiness, cataplexy, and other pathological manifestations of the intrusion of REM sleep-related features into wakefulness [6].
• The results indicate that (1) iontophoretic application of the GABA antagonist bicuculline reversed the typical suppression of neuronal activity seen during slow wave sleep, but had no effect on maintained activity during wakefulness [7].
• Orexin-containing neurons regulate wakefulness, and loss of orexin produces narcolepsy [8].
• The present experiments in 10 adult men were designed to examine whether or not REM sleep inhibits adrenocortical activity and if short periods of wakefulness increase nocturnal cortisol release [9].
• In patients and controls an inverse relationship between plasma AVP concentrations and motor activity during wakefulness was found [10].

High impact information on Wakefulness

• To eat or to sleep? Orexin in the regulation of feeding and wakefulness [6].
• As most of these cells are also inhibited by serotonin but unaffected by histamine, their overall inhibition by transmitters of wakefulness is in agreement with their relative inactivity during waking with respect to sleep [11].
• We also show that these neurons are inhibited by noradrenaline and acetylcholine, both of which are transmitters of wakefulness [11].
• Adenosine: a mediator of the sleep-inducing effects of prolonged wakefulness [12].
• Early morning insomnia, a significant increase in wakefulness during the final hours of drug nights, occurred after 1 or 2 weeks of nightly administration of benzodiazepine hypnotics with short elimination half-lives, when tolerance had begun to develop [13].

Chemical compound and disease context of Wakefulness

• The O2 levels returned to baseline during intermittent wakefulness [14].
• Before medroxyprogesterone therapy, responders were distinguished from nonresponders only by the presence of a significantly lower resting arterial oxygen tension during wakefulness [15].
• Thus, caffeine-induced wakefulness depends on adenosine A2A receptors [16].
• During wakefulness, prolactin and cortisol levels were normal [17].
• The brain targets on which modafinil acts to induce wakefulness, however, remain unknown [18].
• Blockade of dopamine D1 receptors attenuated prolonged wakefulness and synaptic plasticity in these neurons, suggesting that modafinil functions through activation of the dopamine system [19].
• This study suggests that wakefulness per se, independent of respiratory/mechanical stimuli, can influence pharyngeal dilator muscle activity [20].

Biological context of Wakefulness

• Measurements of regional cerebral blood flow (rCBF) by the xenon 133 inhalation method along with polygraph recordings were made serially during relaxed wakefulness and different stages of nocturnal sleep in 18 right-handed normal volunteers [21].
• EMG recording were taken from the posterior cricoarytenoid (PCA) muscles of the larynx during wakefulness and the carbachol-induced, REM sleep-like state [22].
• Normalized inspiratory minute ventilation increased significantly during wakefulness and non-rapid eye movement (non-REM) sleep following each dose of diazepam (p < 0.003 in each case) and following the highest dose during rapid eye movement (REM) sleep (p = 0.01) [23].
• Circadian rhythms in sleep and wakefulness and in salivary melatonin and cortisol concentrations in mothers of term and preterm infants [24].
• Amplitude of ERP (event-related potential) components during wakefulness and sleep were also examined [25].

Anatomical context of Wakefulness

• Monoamine-containing groups that are innervated by orexin neurons do not receive reciprocal connections, while cholinergic neurons in the basal forebrain have reciprocal connections, which might be important for consolidating wakefulness [26].
• Furthermore, infusion of orexin A (1.5 pmol/min) for 6 hr into the lateral ventricle of mice produced a significant increase in wakefulness during the 8 hr after starting infusion to the same level as the wakefulness observed during the active period in wild-type mice, but not at all in H1R gene knockout mice [27].
• Almitrine bismesylate is a peripheral chemoreceptor agonist that improves arterial oxygen tension (PaO2) in patients with COPD during wakefulness [28].
• Interictal spiking during wakefulness and sleep and the localization of foci in temporal lobe epilepsy [29].
• The results emphasize the potential role of dopamine and basal ganglia circuits in the modulation of activated behavioral states (e.g., wakefulness and REM sleep) [30].

Gene context of Wakefulness

• Both OX2R(-/-) and orexin(-/-) mice are similarly affected with behaviorally abnormal attacks of non-REM sleep ("sleep attacks") and show similar degrees of disrupted wakefulness [31].
• Here, we report that a neuropeptide, neuropeptide S (NPS), potently modulates wakefulness and could also regulate anxiety [32].
• Both the top and end hormones of the hypothalamic-pituitary-adrenal axis, i.e. CRH and glucocorticoids, stimulate arousal/wakefulness and inhibit slow wave (deep) sleep in experimental animals and man [33].
• CRH induced an increase in EEG activity in the sigma frequency range, both when it was administered during wakefulness and SWS, while this effect was reduced by pre-treatment with GHRH [34].
• Characterization of ergot and non-ergot serotonin antagonists by prolactin and growth hormone profiles during wakefulness and sleep [35].

Analytical, diagnostic and therapeutic context of Wakefulness

• Microinjection of HA or 2-thiazolylethylamine (an H1-receptor agonist) caused a long-lasting suppression of cortical slow activity and an increase in quiet wakefulness (W) [36].
• We therefore determined waking levels of genioglossus (GG) and tensor palatini (TP) muscle activity (% of maximum electromyographic [EMG] activity) in 10 OSA patients and eight controls, and then assessed the impact of the first two breaths of sleep (theta electroencephalographic [EEG] activity) following a period of stable wakefulness [37].
• Each subject underwent 24-hour holter monitoring for heart rate variability (HRV), an overnight sleep recording, and sodium lactate challenge during wakefulness [38].
• Localized and lateralized cerebral glucose metabolism associated with eye movements during REM sleep and wakefulness: a positron emission tomography (PET) study [39].
• Standard polysomnography of nine normal subjects was recorded for 3 nights (1 adaptation, AD; 1 baseline, BSL; 1 recovery, REC); BSL and REC were separated by a period of 40 h of continuous wakefulness, during which subjects were tested every two hours [40].

References