The neurophysiologic basis of the human sleep–wake cycle and the physiopathology of the circadian clock: a narrative review (original) (raw)

Circadian control of the sleep–wake cycle

Physiology & Behavior, 2007

It is beyond doubt that the timing of sleep is under control of the circadian pacemaker. Humans are a diurnal species; they sleep mostly at night, and they do so at approximately 24-h intervals. If they do not adhere to this general pattern, for instance when working night shifts or when travelling across time zones, they experience the stubborn influence of their circadian clock.

Sleep-wake cycle mechanisms Mecanismos do ciclo sono-vigília

2005

Neurochemically distinct systems interact in the regulation of sleep and wakefulness. Wakefulness is promoted by the aminergic, acetylcholinergic brainstem and hypothalamic systems. Each of these arousal systems supports wakefulness, and coordinated activity is required for alertness and electroencephalogram-proven brain activation. Neurons in the pons and preoptic area control rapid eye movement and non-rapid eye movement sleep. Mutual inhibition among these sleep-wake mechanisms generates behavioral states. An updated understanding of these systems should allow clinicians and researchers to better understand the effects of drugs, injury and neurologic disease on sleep and wakefulness.

Brain mechanisms that control sleep and waking

Naturwissenschaften, 2004

This review paper presents a brief historical survey of the technological and early research that laid the groundwork for recent advances in sleep-waking research. A major advance in this field occurred shortly after the end of World War II with the discovery of the ascending reticular activating system (ARAS) as the neural source in the brain stem of the waking state. Subsequent research showed that the brain stem activating system produced cortical arousal via two pathways: a dorsal route through the thalamus and a ventral route through the hypothalamus and basal forebrain. The nuclei, pathways, and neurotransmitters that comprise the multiple components of these arousal systems are described. Sleep is now recognized as being composed of two very different states: rapid eye movements (REMs) sleep and non-REM sleep. The major findings on the neural mechanisms that control these two sleep states are presented. This review ends with a discussion of two current views on the function of sleep: to maintain the integrity of the immune system and to enhance memory consolidation. This article is based in part on material in the book "The neural control of sleep and waking" (J. Siegel, 2002).

SLEEP-WAKE AS A BIOLOGICAL RHYTHM

Key Words sleep-wake rhythms, free-running rhythms, light, melatonin s Abstract Evidence that the sleep-wake rhythm is generated endogenously has been provided by studies employing a variety of experimental paradigms such as sleep deprivation, sleep displacement, isolating subjects in environments free of time cues, or imposing on subjects sleep-wake schedules widely deviating from 24 hours. The initial observations obtained in isolated subjects revealed that the period of the en-dogenous circadian pacemaker regulating sleep is of approximately 25 hours. More recent studies, however, in which a more rigorous control of subjects' behavior was exerted, particularly over lighting conditions, have shown that the true periodicity of the endogenous pacemaker deviates from 24 hours by a few minutes only. Besides sleep propensity, the circadian pacemaker has been shown to regulate sleep consolidation , sleep stage structure, and electroencephalographic activities. The pattern of light exposure throughout the 24 hours appears to participate in the entrainment of the circadian pacemaker to the geophysical day-night cycle. Melatonin, the pineal hormone produced during the dark hours, participates in communicating both between the environmental light-dark cycle and the circadian pacemaker, and between the circa-dian pacemaker and the sleep-wake-generating mechanism. In contrast to prevailing views that have placed great emphasis on homeostatic sleep drive, recent data have revealed a potent circadian cycle in the drive for wakefulness, which is generated by the suprachiasmatic nucleus. This drive reaches a peak during the evening hours just before habitual bedtime. CONTENTS

Endogenous and exogenous factors on sleep–wake cycle regulation

Progress in Neurobiology - PROG NEUROBIOL, 1999

A number of theories have proposed the involvement of different brain structures and neurotransmitters in order to explain the regulation of the sleep–wake cycle. However, there is no clear consensus as to the mechanisms through which the brain structures and their various neurotransmitters interact to produce theses phases.Perhaps the problem is related to the fact sleep is a very fragile state, easily modified or influenced by a variety of substances or experimental manipulations.In this paper, we describe the evidence of two different groups of factors that induce important changes on the sleep–wake cycle.The endogenous factors: neurotransmitters; hormone; peptides; and some substances of lipidic nature and exogenous factors: stress, food intake, learning, sleep deprivation, sensorial stimulation, exercise and temperature on the regulation the sleep–wake cycle.Likewise, we propose a hypothesis which attempts to reconcile the fact that endogenous and exogenous factors have similar...

Timing of human sleep: recovery process gated by a circadian pacemaker

1984

Timing of human sleep: recovery process gated by a circadian pacemaker DAAN,SERGE,DOMIENG. M. BEERSMA,ANDALEXANDER A. BORB~LY. Timing of human sleep: recovery process gated by a circadian pacemaker. Am. J. Physiol. 246 (Regulatory Integrative Comp. Physiol. 15): Rl61-R178, 1984.--A model for the timing of human sleep is presented, It is

Current understanding on the neurobiology of sleep and wakefulness

The modern concept of sleep and wakefulness has evolved from the landmark discovery of ascending reticular activating system by Moruzzi and Magoun in 1949. The other major contributions have come from the electrophysiological studies of sleep–wake states following the discovery of electroencephalogram by Hans Berger in 1929. Research studies over the past 60 years have provided us an enormous understanding on the neural basis of sleep–wake states and their regulatory mechanisms. By shuttling through the two behavioral states of sleep and wake, brain coordinates many complex functions essential for cellular homeostasis and adaptation to environment. This review brie fl y summarizes the current awareness on the dynamicity of brain mechanisms of sleep and wakefulness as well as the newer concepts of the biological functions of sleep.

Circadian and wakefulness-sleep modulation of cognition in humans

Arousal systems located in the brain stem, basal forebrain (BF) and hypothalamus promote wakefulness while inhibition of these systems promotes sleep ( . Ascending arousal systems are important for activating cortical neurons and promoting cognition. In addition, descending projections from the reticular formation are important for postural control and muscle tone facilitating neurobehavioral output . Neurotransmitters involved in promoting wakefulness include acetylcholine, dopamine, glutamate, histamine, norepinephrine, orexin, and serotonin. Cholinergic cells, located in the pedunculopontine (PPT) and laterodorsal tegmental nuclei (LDT), project to the thalamus and excite thalamocortical cells Frontiers in Molecular Neuroscience www.frontiersin.org April 2012 | Volume 5 | Article 50 | 1

Neurochemical aspects of sleep regulation with specific focus on slow-wave sleep

World Journal of Biological Psychiatry, 2010

The purpose of this review is to outline the mechanisms responsible for the succession of the three vigilance states, namely waking, non rapid eye movement (nonREM) and REM (paradoxical) sleep over 24 h. The latest hypothesis on the mechanisms by which cortical activity switches from an activated state during waking to a synchronised state during nonREM sleep is presented. It is proposed that the activated cortical state during waking is induced by the activity of multiple waking systems, including the serotonergic, noradrenergic, cholinergic and hypocretin systems located at different subcortical levels. In contrast, the neurons inducing nonREM sleep are all localized in a single small nucleus named the ventrolateral preoptic nucleus (VLPO) situated above the optic chiasm. These neurons all contain the inhibitory neurotransmitter γ -aminobutyric acid. The notion that the switch from waking to nonREM sleep is due to the inhibition of the waking systems by the VLPO sleep-active neurons is introduced. At the onset of sleep, the sleep neurons are activated by the circadian clock localized in the suprachiasmatic nucleus and a hypnogenic factor, adenosine, which progressively accumulates in the brain during waking. World J Biol Psychiatry Downloaded from informahealthcare.com by University Claude Bernard Lyon 1 on 07/30/10 For personal use only.