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(Stage W)

Alpha and Beta-activity
--> Beta activity is desynchronized



- reflects the fact that many different neuronal circuits are actively processing information

- occurs when a person is alert

--> Beta-activity


Stage 1 sleep (NREM 1)


--> firing of neurons in the neocortex is becoming more synchronized

Transition between sleep and wakefulness



Stage 2 Sleep (NREM 2)

Theta activity

Sleep spindles: play a role in consolidation of memories

K-complexes: triggered by noises

(15 min)



- triggered by noises/occur in response to a stimulus

- large waveforms in EEG

- forerunner of delta waves


Sleep spindles

play a role in the consolidation of memories

--> short bursts of waves


Stage 3 Sleep (NREM 3)
Slow wave sleep


deepest stage of sleep
--> only loud noises can cause people to wake up
--> when woken up, people are groggy and confused

(60 min)



Theta and Beta-activity

person is paralyzed at this stage, because spinal and motor neurons are strongly inhibited
--> one does not react to loud noises, just meaningful stimuli (e.g. name)

when woken up, people are alert and attentive


Functions of slow wave sleep

- brain rests

- Recovery
--> regions that had highest waves (most active) during wakefulness, have the highest waves during slow wave

- low metabolic rate
--> permits restorative mechanisms to destroy free radicals

- facilitates the consolidation of declarative memories


Effects of sleep deprivation

- cognitive abilities are effected
--> perceptual distortions
--> hallucinations
--> trouble concentrating

- one never regains all the sleep one lost

- causes increase in free radicals


Free radicals

- unstable molecules that can damage the cells in the body
--> form when atoms or molecules gain or lose electrons

- accumulate during waking

- contain at least one unpaired electron


Oxidative Stress

1. When the body uses oxygen it produces free radicals as a by - product

2. Free radicals then bind with the oxygen molecules which results in them splitting into single atoms

--> this causes oxidative stress


Fatal familial insomnia

damage to portions of the thalamus
--> disappearance of slow wave sleep + only brief episodes of REM sleep without paralysis


Functions of REM Sleep

promotes brain development

- facilitates the consolidation of nondeclaractive memories


Rebound Phenomenon

After sleep deprivation

--> when permitted to sleep normally there is a higher-than normal percentage of REM sleep in the recovery night


Nondeclarative memories

Memories gained through experience + practice

(e.g.: learning to drive a car, recognizing a face, throw a ball)


Declarative memories

Memories of past episodes of ones life, memories one can talk about

Memories of the relationships between a stimuli or events



- sleep promoting substance that accumulates during waking and is destroyed during sleep

- plays the primary role in the control of sleep


Neural control of sleep

1. Prolonged wakefulness results in a decrease of glycogen
--> fuel for neurons, produced by astrocytes

2. Increase of extracellular adenosine
--> inhibitory effect on neural activity

3. Accumulation of adenosine promotes sleep

4. During slow wave
--> neurons rest
--> adenosine decreases
--> Astrocytes renew the stock of glycogen


Role of caffeine

- antagonist

- blocks adenosine receptors to prevent sleepiness

- only works when there is actual sleep deprivation


Neural control of arousal
--> What are the systems involved ?

Five systems of neurons are of importance for alertness and wakefulness

--> Acetylchonergic System
--> Norodrenergic System
--> Serotonergic System
--> Histaminergic System
--> Orexinergic System


Acetylchonergic System

- 2 groups of ACh neurons are located in pons + basal forebrain

- 1 group is located in the medial septum
--> controls the activity of the hippocampus

=> high levels of ACh in those regions during
--> REM
--> waking


Norodrenergic System

- located in the locus coeruleus ( dorsal pons )

- stimulation causes immediate waking ( vigilance )

=> high firing rate during
--> waking


Serotonergic System

- located in the raphe nuclei ( reticular formation )

- stimulation causes locomotion and cortical arousal

=> high firing rate during
--> wakefulness


Histaminergic System

- located in the tuberomammilary nucleus ( TMN ) of the thalamus

- axons project amongst other regions to cerebral cortex and basal forebrain
--> increase of cortical arousal due to the release of ACh

=> control of wakefulness is shared with other neurotransmitters


Orexinergic System

- located in the lateral hypothalamus

- axons project to all of the regions where the other systems for alertness are located

--> has an excitatory effect on all of the other regions, thus causes the release of their neurotransmitters

=> high firing rate during wakefulness


Homoestatic control

Mainting the balance of sleep/wake at an optimal level


Allostatic control

reactions to stressful events, that serve to override homoestatic control

ex.: in case of danger one is more alert/high attentive even if one is sleep deprived


Cicardian Control

Entraining periods of sleep to particular portions of light/dark cycle


Preoptic Area

- suppresses the activity of the arousal neurons when active
--> most involved area in sleep