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What Part Of The Brain Controls Sleep And Arousal

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The Ascending Arousal System Induces Wakefulness

Hypothalamus – Human Brain Series – Part 17

Contemporary models of the wake-sleep regulatory system are based on the seminal research conducted by von Economo, Moruzzi, and Magoun. In 1930, von Economo reported that a viral illness known as encephalitis lethargica was caused by lesions of the posterior hypothalamus and rostral midbrain . Consequently, he hypothesized that wakefulness is mediated by an ascending arousal system beginning in the brainstem, which remains active following midbrain interruption of the classical sensory pathways.

A schematic drawing showing key components of the ascending arousal system. Adapted from Saper 2005, pg 1258 .

In sum, cholinergic neurons, monoaminergic cell populations, and orexin/hypocretin nuclei of the lateral hypothalamus located along the two branches of the ascending arousal system, discharge in a stereotypical and coordinated manner to promote cortical arousal, with each making unique, though overlapping and redundant, contributions to achieve and sustain wakefulness. During sleep, these circuits are blocked by neurons of the VLPO.

Frontiers In Computational Neuroscience

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What Your Brain Does While You Sleep

  • Sleep Stage 1: As you enter this first stage of sleep, your brain slowly changes from wakefulness to sleep. If there is a change in your surroundings, you are likely to wake up.
  • Sleep Stage 2: Your heart rate and brain waves slow during stage 2 sleep, preparing your mind and body for restorative deep sleep.
  • Sleep Stage 3: During stage 3 sleep, your brain waves reach their lowest frequency, and it would be hard for anything to disturb your slumber. As a result, stage 3 sleep is also known as slow wave sleep or deep sleep. How much deep sleep you get will dictate how well-rested you feel come morning.
  • REM Sleep: Finally, you reach the final stage of sleep: rapid eye movement sleep . Your brain is the most active that it will be as you sleep. According to the National Institutes of Health, most of your dreams will occur now as your body is temporarily paralyzed. This sleep stage is pivotal for your memory and learning potential.

This cycle will take around 90 minutes. After you complete your first cycle, it will start over again.

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Sleep Anesthesiology And The Neurobiology Of Arousal State Control

Ralph Lydic, Helen;A. Baghdoyan; Sleep, Anesthesiology, and the Neurobiology of Arousal State Control. Anesthesiology 2005; 103:12681295 doi:

Sleep, like breathing, is a biologic rhythm that is actively generated by the brain. Neuronal networks that have evolved to regulate naturally occurring sleep preferentially modulate traits that define states of sedation and anesthesia. Sleep is temporally organized into distinct stages that are characterized by a unique constellation of physiologic and behavioral traits. Sleep and anesthetic susceptibility are genetically modulated, heritable phenotypes. This review considers 40 yr of research regarding the cellular and molecular mechanisms contributing to arousal state control. Clinical and preclinical data have debunked and supplanted the primitive view that sleep need is a weakness. Sleep deprivation and restriction diminish vigilance, alter neuroendocrine control, and negatively impact immune function. There is overwhelming support for the view that decrements in vigilance can negatively impact performance. Advances in neuroscience provide a foundation for the sea change in public and legal perspectives that now regard a sleep-deprived individual as impaired.

Homeostatic Regulation Of Sleep/wake States

Parts of the brain and psychology methods

When wakefulness is extended, sleep pressure accumulates and only dissipates during subsequent sleep. This homeostatic process was initially modeled three decades ago by Borbely in the two-process model of sleep regulation . According to this model, sleep pressure increases during wakefulness and declines during sleep in a cycle superimposed over the circadian cycle of activity . While this model has been highly influential, the neuronal substrate of Process S still remain elusive. More than a century ago, researchers revealed that the cerebrospinal fluid of sleep deprived animals contained substances that can promote sleep in other animals . This finding led to the premise that wake-dependent homeostatic substances accumulate with wakefulness, and when sensed by a homeostatic system promote sleep. Among the homeostatic substances and mechanisms suggested are adenosine and its receptors A1 and A2A, cytokines such as interleukin-1 and tumor necrosis factor-, prostaglandin D2, and Nitric oxide . Nonetheless, it is still unclear how the brain senses and responds to sleep need, where in the brain this process takes place, and whether lack of sleep is sensed by a master control center or by various regulatory neuronal networks. These remain central questions in sleep neurobiology .

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Ascending Reticular Activating System

The ascending reticular activating system consists of a set of neural subsystems that project from various thalamic nuclei and a number of dopaminergic, noradrenergic, serotonergic, histaminergic, cholinergic, and glutamatergic brain nuclei. When awake, it receives all kinds of non-specific sensory information and relays them to the cortex. It also modulates fight or flight responses and is hence linked to the motor system. During sleep onset, it acts via two pathways: a cholinergic pathway that projects to the cortex via the thalamus and a set of monoaminergic pathways that projects to the cortex via the hypothalamus. During NREM sleep this system is inhibited by GABAergic neurons in the ventrolateral preoptic area and parafacial zone, as well as other sleep-promoting neurons in distinct brain regions.

Historical Development Of The Stages Model

The stages of sleep were first described in 1937 by Alfred Lee Loomis and his coworkers, who separated the different electroencephalography features of sleep into five levels , representing the spectrum from wakefulness to deep sleep. In 1953, REM sleep was discovered as distinct, and thus William C. Dement and Nathaniel Kleitman reclassified sleep into four NREM stages and REM. The staging criteria were standardized in 1968 by Allan Rechtschaffen and Anthony Kales in the “R&K sleep scoring manual.”

In the R&K standard, NREM sleep was divided into four stages, with slow-wave sleep comprising stages 3 and 4. In stage 3, delta waves made up less than 50% of the total wave patterns, while they made up more than 50% in stage 4. Furthermore, REM sleep was sometimes referred to as stage 5. In 2004, the AASM commissioned the AASM Visual Scoring Task Force to review the R&K scoring system. The review resulted in several changes, the most significant being the combination of stages 3 and 4 into Stage N3. The revised scoring was published in 2007 as The AASM Manual for the Scoring of Sleep and Associated Events. Arousals, respiratory, cardiac, and movement events were also added.

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The Case Of Henry Molaison

In 1953, Henry Gustav Molaison was a 27-year-old man who experienced severe seizures. In an attempt to control his seizures, H. M. underwent brain surgery to remove his hippocampus and amygdala. Following the surgery, H.Ms seizures became much less severe, but he also suffered some unexpectedand devastatingconsequences of the surgery: he lost his ability to form many types of new memories. For example, he was unable to learn new facts, such as who was president of the United States. He was able to learn new skills, but afterward he had no recollection of learning them. For example, while he might learn to use a computer, he would have no conscious memory of ever having used one. He could not remember new faces, and he was unable to remember events, even immediately after they occurred. Researchers were fascinated by his experience, and he is considered one of the most studied cases in medical and psychological history . Indeed, his case has provided tremendous insight into the role that the hippocampus plays in the consolidation of new learning into explicit memory.

Information Systems And Functional Genomics Of Arousal State Control

Arousal Stimulation – Brain Manipulation with Iso Chronic Tones & Binaural Beats

The ability to create in real time a complete, digital, anesthesia record offers a powerful tool for translational research. The large amount of human physiologic information that can be synthesized by digital information systems has the potential to provide anesthesiology with unique patient data for phenotyping comorbidities. These information systems also give anesthesiology a special opportunity for developing a functional genomics that can link genetic factors to anesthesia outcome.

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Components Of The Brainstem

The three components of the brainstem are the medulla oblongata, midbrain, and pons.

Brainstem Anatomy: Structures of the brainstem are depicted on these diagrams, including the midbrain, pons, medulla, basilar artery, and vertebral arteries.

The medulla oblongata; is the lower half of the brainstem continuous with the spinal cord. Its upper part is continuous with the pons. The medulla contains the cardiac, respiratory, vomiting, and vasomotor centers regulating heart rate, breathing, and blood pressure.

The midbrain is associated with vision, hearing, motor control, sleep and wake cycles, alertness, and temperature regulation.

The pons lies between the medulla oblongata and the midbrain. It contains tracts that carry signals from the cerebrum to the medulla and to the cerebellum. It also has tracts that carry sensory signals to the thalamus.

Neurons Utilizing Neuromodulators Regulate Arousal And Sleep Circuits

Since early pharmacological studies followed by histochemical and then specific lesion studies pioneered by Jouvet, the important role of ACh and monoamines as neuromodulators in wake-sleep states was revealed in the last century . Indeed, in these original studies, it was believed that the neuromodulatory systems could generate the sleep-wake states.

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The Neuropathology Of Sleep

At present, the pathophysiology of many sleep-wake disorders is poorly understood . Generally, a combination of biological, psychological, and social factors is implicated in the etiology of these conditions. The remainder of this review will describe the substrates and mechanisms that have been identified in the most common sleep-wake disorders and the clinical implications for the selection of suitable treatment strategies.

Mammalian Neuronal Circuitry Of Sleep/wake States

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How does the mammalian brain control sleep and wakefulness? It is currently understood that complex interactions between subcortical neuromodulatory neurons in the brainstem, midbrain, hypothalamus, and basal forebrain , the thalamus, and the cortex drive behavioral, physiological, and electrocortical sleep/wake states. Wake-promoting populations project to various structures through a dorsal and a ventral pathway. The dorsal pathway innervates the thalamuswhich facilitates transmission of sensory information to the cortex. The ventral pathway innervates the hypothalamus, BF, and other forebrain structureswhich together excite the cortex. It is thought that wakefulness is achieved when both the dorsal and the ventral pathways are activated. In this review, we will mainly focus on wake-promoting neuronal circuits, as excellent recent reviews have covered the neuronal mechanisms underlying NREM and REM sleep .

Figure 1

Schematic of neuronal wake-promoting populations. BF, basal forebrain; DA, dopamine; DR, dorsal raphe; Hcrt, hypocretin; His, histamine; LC, locus coeruleus; LH, lateral hypothalamus; NA, noradrenaline; PB, parabrachial area; PPT/LDT, pedunculopontine and laterodorsal tegmental nuclei; TMN, tuberomammillary nucleus; VTA, ventral tegmental area.

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Traits Defining States: Respiration

Sleep apnea comprises one of the most prevalent and poorly understood sleep disorders. The apneic episodes illustrated by are more frequent and of longer duration during REM sleep., Anesthesia depresses upper airway muscle function, and this depressant action is more severe in the upper airway than on the phrenic nerve. These data make sleep apnea directly relevant for efforts to maintain airway patency before and after intubation associated with anesthesia or sedation.,,;

Fig. 8. Polygraphic recording of human sleep and breathing.; A;shows a transition into rapid eye movement sleep. The; arrow;; B;shows a 30-s record obtained from a patient during a prolonged apnea. Note the cessation of nasal/oral airflow and the prolonged interval of hypopnea. During an arousal , muscle tone , respiratory effort , and airflow resumed. This recording illustrates the point that individuals with sleep apnea must awaken to terminate an airway obstruction and successfully breathe. Abd 1/2 = respiratory effortabdomen; C3/A2 = left central electroencephalogram; EKG1/2 = electrocardiogram; Snor1/2 = snoring sensor; LAT1/2 = left anterior tibialis electrocardiogram; LOC-A2 = left outer canthus/right ear lobe electrooculogram placement; Nasal/Oral = airflow from nasal/oral cavity; O1/A2 = left occipital electroencephalogram; RAT1/2 = right anterior tibialis electrocardiogram; ROC-A2 = right outer canthus/right ear lobe electrooculogram placement; Thor1/2 = respiratory effortchest.;

Why Is This Useful

For people in an unconscious state that are unable to wake up, there may be a possibility for some sort of therapy as scientists start understanding what parts of the brain control consciousness and thus, what parts to target. This would be similar to the way deep brain stimulation is currently being experimented with as a treatment for Parkinsons Disease.

It also might be possible to stimulate some parts of the brain to address depression as well as a variety of consciousness disorders.

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Multiple Traits Define Arousal States

The success of sleep neurobiology has been derived, in part, from deconstructing states into their component traits and then characterizing the mechanisms regulating those traits. Those data, and the lack of support for a unitary hypothesis of anesthesia,, make clear that characterizing the mechanisms generating anesthetic traits provides a powerful paradigm for gaining insight into the regulation of anesthetic states. The desirable anesthetic state is a constellation of reversible traits that include analgesia, amnesia, unconsciousness, blunted sensory and autonomic reflexes, and skeletal muscle relaxation. In addition to the characteristic of reversibility, another goal of anesthesia is the temporal coordination of the foregoing five traits. Ideally, the onset of these drug-induced traits occurs at approximately the same time. Undesirable anesthetic complications often are characterized by temporal dissociations in the offset of drug-induced traits, such as failure of a seemingly awake, postanesthetic patient to maintain upper airway patency. As with successful anesthesia, normal sleep also requires the temporal coordination of multiple traits. In fact, the nosology of many sleep disorders is characterized by the intrusion of sleep traits into the state of wakefulness or the expression of waking traits during sleep .

The Dorsal Raphe Nucleus/ventral Periaqueductal Gray

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The DRN is a heterogeneous brainstem nucleus that innervates many brain regions implicated in sleep/wake regulation. DRN neurons express various neurotransmitters, including serotonin and dopamine. DRN serotonin neurons were initially hypothesized to play an important role in the initiation and maintenance of NREM sleep, as lesions to the DRN in rats and cats resulted in insomnia . Nonetheless, further examinations of the activity pattern of serotonergic DRN neurons across arousal states revealed that they are wake-active and predominantly silent during NREM and REM sleep . Later work suggested that serotonergic DRN neurons facilitate quiet wakefulness and inhibit REM sleep . Further cell type, receptor- and projection-specific functional interrogations of serotonergic DRN circuitry are required to reveal the casual role of this population in sleep/wake regulation.

It is important to note that not all dopaminergic populations promote wakefulness, as SNc dopaminergic neurons projecting to the dorsal striatum have been suggested to promote NREM sleep . It would be of interest for future studies to determine the functional role of additional dopaminergic populations, including the caudal hypothalamic A11, arcuate nucleus A12 and the zona incerta A13 groups. In addition, it would be useful to determine whether dopaminergic neurons act in concert or independently to generate, regulate, and/or maintain sleep and wake states.

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Understanding how the brain controls arousal could help researchers design new sleep and anesthetic drugs that create a state more similar to natural sleep. Stimulating the TRN can induce deep, non-REM-like sleep states, and previous research by Brown and colleagues uncovered a circuit that turns on REM sleep.

Brown adds, The TRN is rich in synapses connections in the brain that release the inhibitory neurotransmitter GABA. Therefore, the TRN is almost certainly a site of action of many anesthetic drugs, given that a large classes of them act at these synapses and produce slow waves as one of their characteristic features.

Previous work by Lewis and colleagues has shown that unlike the slow waves of sleep, the slow waves under general anesthesia are not coordinated, suggesting a mechanism for why these drugs impair information exchange in the brain and produce unconsciousness.

Anne Trafton MITImage Credit: The image is credited to Jose-Luis Olivares/MITOriginal Research:Abstract for Thalamic reticular nucleus induces fast and local modulation of arousal state by Laura D Lewis, Jakob Voigts, Francisco J Flores, Lukas I Schmitt, Matthew A Wilson, Michael M Halassa, and Emery N Brown in eLife. Published online October 12 2015 doi:10.7554/eLife.08760


Thalamic reticular nucleus induces fast and local modulation of arousal state

Hypothalamic Modulation Of Rem Sleep

Descending inputs from sleep and arousal regulatory hypothalamic neuronal systems are sources of modulatory control of REM sleep circuits. The HCT peptides have REM-suppressing effects. HCT receptor antagonists augment REM sleep . Optogenetic activation of HCT neurons during either NREM or REM sleep evokes waking . HCT neurons target key nodes in brain stem REM sleep circuitry including neurons in the vlPAG/LPT, DRN, and LC. Activation of HCT neurons during waking suppresses manifestations of REM sleep, and REM-generating circuits;are disinhibited during NREM sleep;when HCT neuronal activity;is minimal.

Neurons expressing the inhibitory peptide melanin-concentrating hormone are localized in the lateral hypothalamus, zona incerta, and dorsomedial hypothalamus . Included among the targets of MCH neurons are LC, DRN, and vlPAG. MCH neurons also express GABA. MCH neurons are nearly silent during waking, seldom discharge during NREM sleep, and are most active during REM sleep . Expression of c-Fos in MCH neurons is increased during REM-enriched sleep following prolonged REM sleep deprivation . Optogenetic activation of MCH neurons during NREM sleep significantly increases the probability of transitions to REM sleep . Mechanisms of MCH REM sleep enhancement involve disinhibition of SLD REM on neurons via MCH/GABA inhibition of REM off neurons in the TMN, vlPAG, DRN, and LC .

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