Sleep
It is late in winter, and many parts of Acta Physiologica’s countries of origin are still covered by a blanket of snow, which brings with it a desire for rest and hibernation that tends to spill over from the animal kingdom to the authors' desks.
Abstract
It is late in winter, and many parts of Acta Physiologica’s countries of origin are still covered by a blanket of snow, which brings with it a desire for rest and hibernation that tends to spill over from the animal kingdom to our desks. Although as human beings, we are not, or no longer, permitted to sleep away the twilight times of the year, recurring circadian sleep is, and will probably be for a long time, a prerequisite for human life as we know it. Night time sleep is a great example of adaptation to life on a planet that revolves around the sun. Hypnograms depicting the sleep cycles of individuals have not only shown us the well-known sleep stages and cycles, but have let us learn that sleep patterns are, on the one hand, very individual, while at the same time stable from one night to the next (Porkka-Heiskanen et al. 2013). The questions of why we sleep and what strange realities our minds enter in our dreams will probably have troubled our ancestors from early on (Scully 2013). Assumably, the imperative need for sleep and the deleterious consequences of sleep deprivation will have been experienced even earlier. And, astonishingly, the jury is still out on those questions today. Nevertheless, we keep learning the details of how sleep is controlled by the human body: apparently, a tightly controlled interplay of biochemical signals between remote parts of the brain lets us go to sleep and back (Scully 2013). Wake signals are currently being attributed to upper pontine cholinergic neurones that activate the thalamus (Peplow 2013). Thalamus, from Greek ‘hάkalος’ or ‘inner chamber’, has been labelled the ‘Gate to Consciousness’ for its channelling function between sensory areas and the cortex (Pape et al. 2005, Peplow 2013). Hypothalamic orexins foster the wake signals of the ascending arousal system, which includes several areas of the brain and a multitude of neurotransmitters such as serotonin, histamine, dopamine and noradrenaline (Stj€arne & Persson 2012). It has been postulated that metabolic processes convey the information of ‘tiredness’ through ATP breakdown products to the ventrolateral pre-optic nuclear area of the hypothalamus (VLPO). VLPO closely communicates with the suprachiasmatic nucleus, which in turn receives circadian control signals from the retina (light signals) and the pineal gland (melatonin; Nduhirabandi et al. 2013), enabling VLPO to, if need be, induce sleep by inhibiting the arousal system through GABA/galaninergic signalling (Peplow 2013). Recent advances have let us understand, for example, the role of midbrain GABAergic signalling (Lahti et al. 2013) and the workings of the circadian clock, which regulates many more physiological functions than the activity state of the brain (P acha & Sumov a 2013) and which, in turn, is influenced by various environmental stimuli (Egg et al. 2013). Both the quality and the quantity of sleep that an individual gets determine the risk of developing complex disease entities such as metabolic or immune system disorders as well as neurodegenerative disease. It has been postulated that modern-day environments, which let us switch on the light and have a cup of coffee almost when and wherever we want to, interfere with healthy sleep patterns. Caffeine is no longer a luxury of the wealthy or a substance ordered from the pharmacy to study calcium release (Lally et al. 2012, Cheong & Shin 2013), but the most common drug, ever. Most of you will probably guess who the world leaders in caffeine intake currently are. Recent results (many of which have undoubtedly been produced in artificially lit labs by caffeine-devouring scientists long after dark) help us understand both the complex relations between sleep, obesity, cardiovascular disease, the endocrinum and the mood (Porkka-Heiskanen et al. 2013, DeWeerdt 2013), as well as disease entities such as enuresis (Osman et al. 2013, Nev eus & Sill en 2013) (Griffiths & Fowler 2013, de Groat & Wickens 2013) or sleep apnoea (Tan et al. 2013) that disturb a child’s sleep during developmental phases in which the consolidating function that sleep exerts on the memory is absolutely critical (Peplow 2013, Smith 2013). Side effects of medical treatment strategies of insomnia are well known and debated (Scully 2013), and new strategies are highly due. New pharmacological agents are currently being validated that do not only affect mental wakefulness, but interfere with the pathological metabolic effects resulting from, among others, disturbed sleep patterns (Kirilly et al. 2012). Sleep disturbances have increasingly, and often in previously unexpected contexts, been shown to be