Neurobiology of sleep (Review)

Abstract

Sleep is a physiological global state composed of two different phases: Non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. The control mechanisms of sleep manifest at the level of genetic, biological and cellular organization. Several brain areas, including the basal forebrain, thalamus, and hypothalamus, take part in regulating the activity of this status of life. The signals between different brain regions and those from cortical areas to periphery are conducted through various neuromediators, which are known to either promote wakefulness or sleep. Among others, serotonin, norepinephrine, histamine, hypocretin (orexin), acetylcholine, dopamine, glutamate, and gamma-aminobutyric acid are known to orchestrate the intrinsic mechanisms of sleep neurobiology. Several models that explain the transition and the continuity between wakefulness, NREM sleep and REM sleep have been proposed. All of these models include neurotransmitters as ligands in a complex reciprocal connectivity across the key-centers taking part in the regulation of sleep. Moreover, various environmental cues are integrated by a central pacemaker-located in the suprachiasmatic nucleus-which is able to connect with cortical regions and with peripheral tissues in order to promote the sleep-wake pattern. Contents

The Interplay Between Neuroinfections, the Immune System and Neurological Disorders: A Focus on Africa

“…Sleep is a complex physiologic, recurring, and reversible state of decreased metabolism, responsiveness to external stimuli, and motor activity regulated by a circadian rhythm ( 172 – 174 ). The neurophysiological stages of sleep can be evaluated using polysomnography (PSG), which incorporates EEG for brain electrical activity, electromyogram (EMGs) measuring muscle tone, and electrooculograms (EOGs) that assess eye movement ( 20 , 175 ).…”

Ischemic Stroke and Sleep: The Linking Genetic Factors

“…COMT gene (Val158Met) was shown to be associated with post-stroke functional recovery, and Met allele has a prognostic value in Korean population with the better prognosis for COMT Met (-) (Val/Val alleles carriers). Substitution of Val to Met leads to the decreased enzyme activity of COMT and accumulation of synaptic dopamine [72]. Dopaminergic system interacts with the circadian PER genes, normal rhythmic expression of PER2 in the striatum depends on the dopamine and dopamine receptors (D2), and can be involved in circadian rhythm disruption in neurological disorders.…”

“…Several neurotransmitter systems are involved in sleep–wake regulation and include wake-promoting substances [serotonin, norepinephrine (NE), histamine, hypocretins, acetylcholine (ACh), dopamine, glutamate, and gamma-aminobutyric acid (GABA)] and sleep-promoting factors (melanin-concentrating hormone, adenosine, and several cytokines) [ 72 ]. The genes encoding the components of these neurotransmitter systems are compelling candidates linking sleep disorders and cerebrovascular disease.…”

“…COMT gene (Val158Met) was shown to be associated with post-stroke functional recovery, and Met allele has a prognostic value in Korean population with the better prognosis for COMT Met (–) (Val/Val alleles carriers). Substitution of Val to Met leads to the decreased enzyme activity of COMT and accumulation of synaptic dopamine [ 72 ].…”

Methylmercury plus Ethanol Exposure: How Much Does This Combination Affect Emotionality?

“…[ 92 ]. In a canonical pathway, reduction of luminosity, levels of substances on blood and brain (glucose, cortisol, adrenaline, among others), release of melatonin, followed by increases in GABAergic and galanin transmission results in the end of the wake phase [ 92 , 93 , 94 ]. On the other hand, imbalance on activity of other regulators such as serotonin, noradrenalin, dopamine, histamine, and glutamate also may result in sleep disturbance [ 94 , 95 ].…”