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Sleep stages and circadian rhythms - Processing the Environment - MCAT - Khan Academy

Research findings suggesting that sleep loss and anxiety are closely linked were among those presented at Neuroscience , the annual conference of the Society for Neuroscience held in San Diego, California. Poor sleep seems to put the brain on-guard by triggering spikes in stress hormones like cortisol, producing an early a.

The conditions fuel each other, with compounding effects. Thankfully, science is also serving up some good news with practical applications.

Sleep as an Adaptive Process

And the really good news is that many of the negative effects of sleep loss appear reversible after just one night of peaceful sleep. Most researchers agree that sleep may be especially important for restoring the brain and provide something not afforded by quiet waking, but there is great uncertainty when it comes to which chemical or molecular pathway in the brain may be wasted during waking and restored during sleep.

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Memory consolidation and brain restitution are important perspectives on the function of sleep that are not mutually exclusive. The synaptic homeostasis hypothesis reconciles these two perspectives by proposing that the main function of sleep is to control the strength of synapses impinging on neurons in the cortex and elsewhere. At the same time, the hypothesis claims that sleep is the price we pay because our brains are plastic, and is thus related in an important manner to memory.

Finally, since sleep is especially abundant early in development when intense synaptic remodeling occurs, I will discuss recent studies linking sleep and brain maturation.


Sleep timing and sleep structure are regulated by a fine-tuned interaction of circadian rhythmicity and sleep homeostasis. Various aspects of sleep, e.

Sleep and circadian rhythmicity also contribute to human brain functioning during wakefulness. Effects of circadian rhythmicity and sleep homeostasis can be observed at the level of behaviour, electrophysiology and fMRI assessed brain responses. I will discuss how these contributions vary across cognitive domains, brain regions, between individuals and genotypes and change with age.

The amount and macrostructure of sleep, as well as the major electrophysiological characteristics of sleep, like spindles and slow waves detected with the EEG, change significantly during development.

BMS Neuroscience of sleep - Prospectus Faculty of Medical Sciences

These EEG modifications seem to reflect changes of key neural network properties during development. Changes in sleep spindles Hz , which are generated by the thalamo-cortical system, are closely related to measures of cognitive performance. Changes in sleep slow waves 0. Numerous studies show that sleep, in particular sleep slow waves and spindles, play an important role in learning related cortical plasticity. Thus, manipulations during sleep can be used to actively and non-invasively change brain connectivity.

Neuroscience of sleep

Finally, the developmental trajectory of key aspects of sleep can be used to study clinical populations. For example, the spatial distribution of slow waves during sleep shows a maturational delay in children with attention deficit hyperactivity disorder. Moreover, the disruption of normal slow waves in children with continuous spike wave epilepsy during slow wave sleep may be related to neurocognitive regression. Children spend half of their lives asleep: thus, a focus on waking development may be too one-dimensional. In fact, the great sleep need in early human life may further support that sleep plays a critical role in processes of brain maturation.

The circuitry in the brain that regulates sleep and wakefulness was first addressed by the Baron Constantin von Economo, based on his observations on human subjects with pathological lesions of this circuitry.

The Neuroscience of Sleep

Recent advances have confirmed the overall plan that von Economo proposed, but identified many novel sites that promote either sleep or wakefulness. I will review these systematically emphasizing particularly recent evidence from opto- and chemogenetic manipulation of these circuits, and in particular emphasize a new model, in which the key wake-sleep regulatory circuits use excitatory or inhibitory amino acid neurotransmitters, rather than either monoamines or peptides, which appear to play a modulatory role.

I will first consider wake-promoting circuitry, reviewing the key roles played by glutamatergic neurons in the parabrachial and pedunculopontine nuclei in the brainstem and in the supramammillary nucleus in the hypothalamus, as well as by GABAergic neurons in the basal forebrain and the supramammillary nucleus. I will also consider the roles played by monoaminergic neurons in the brainstem and hypothalamus, cholinergic neurons in the pedunculopontine nucleus and basal forebrain, and peptidergic neurons in the lateral hypothalamus. Finally I will discuss recent evidence for two wake-promoting GABAergic pathways from the lateral hypothalamus that inhibit sleep-promoting targets.

I will then consider sleep-promoting cell groups, which use GABA to inhibit wake-promoting targets. These include the ventrolateral and median preoptic nuclei and the parafacial zone in the pons. I will also discuss the role of the melanin-concentrating hormone neurons in the lateral hypothalamus in REM sleep regulation, and recent evidence that they may release both GABA and glutamate. Finally, I will consider how these basic wake and sleep circuits interact with each other, and how they are controlled by homeostatic and circadian drives.

Slow waves, the hallmark of NREM sleep, are not uniformly distributed across the cortical surface, but can occur locally and asynchronously across brain regions. Their regional distribution and amplitude is affected by brain maturation and by time spent awake, and mediated in part by experience-dependent changes. Regional changes in slow waves and sleep spindles reflect the off-line processing and transformation of wake-dependent brain modifications, in line with a direct involvement of sleep in learning and memory consolidation.

On the other hand, local wake-like activity may occur during sleep and has been suggested to be involved in the generation and characterization of dream experiences.