Stages of sleep: electrodes monitor EEG, muscle activity recorded as electromyogram EMG, eye
movement recorded as electro-oculogram EOG. During wakefulness, there is alpha activity: regular,
medium-frequency waves 8-12 Hz, eyes closed. Beta activity is irregular, low amplitude waves 13-30 Haz,
shows desynchrony – many neural circuits actively processing info, person alert and attentive. Stage 1:
theta activity, transition between sleep/wakefulness, eyes open/close, roll up/down. After 10 minutes, stage
2: EEG irregular w/ some periods of theta activity, sleep spindles (short bursts of waves 12-14 Haz, fewer in
older people), K complexes (sudden, sharp waveforms, only during stage 2, spontaneously occur once a
minute, can be triggered by noises, forerunner of delta waves. Person does not feel asleep. After 15 minutes,
stage 3 has high-amplitude delta activity, 3.5 Hz, also in stage 5. After 45 minutes of stage 4, EEG becomes
desynchronizes, some theta waves, eyes rapidly move, person paralyzed – REM sleep. 1-4 are non-REM.
3-4 are slow-wave b/c of delta activity. Cycles are 90 minutes long, 20-30 minutes REM, becomes longer,
more REM and stage 2. Basic rest-activity cycle: 90 minutes cycle of waxing and waning alertness,
controlled by biological clock in caudal brain stem, controls REM cycles and slow-wave sleep. During
REM we are paralyzed, but brain very active – accelerated cerebral blood flow, oxygen consumption
Mental activity during sleep: during REM, rate of cerebral blood flow is high in visual association cortex
but low in primary visual and prefrontal cortex, b/c eyes not receiving visual input but still have visual
hallucinations. Dreams have good images but poor organization. Eye movements related to what is
happening during dream. EEG wave not produced by eye movements; indicates subjects scanning imaginary
visual image during dream. Some brain mechanisms that become active during dream are those that become
active if events actually happened. Nightmares mostly during stage 4.
Insomnia: affects 25% occasionally, 9% regularly. Defined relative to person’s particular sleep needs.
Insomnia is not a disease, it is a symptom. Drug dependency insomnia: caused by side effects of
increasing doses of sleeping medications. Most people underestimate amount of time they actually sleep,
and medication doesn’t help much except short-term, often based on personality. Drugs that increase sleep
time but cause hangover in the morning are useless, better to have hangover-fere drugs. Sleep apnea:
inability to breathe and sleep at the same time. CO2 level in bood stimulates chemoreceptors and person
Narcolepsy: neurological disorder , sleep at inappropriate times, primary symptom is sleep attack for 2-5
minutes, wake up feeling refreshed. Cataplexy: complete paralysis during waking, usually follows strong
emotional reactions / physical effort. Sleep paralysis: inability to move just before onset of sleep or upon
waking in morning. Hypnagogic hallucinations: vivid dreams occur just before person falls asleep,
accompanied by sleep paralysis. Narcolepsy caused by brain abnormality that disrupts neural mechanisms
controlling aspects of sleep/arousal. Skip slow-wave sleep directly to REM, sleep disrupted by wakefulness,
difficulty staying awake. Genetic disorder, influenced by unknown enviro factors. Dog study showed it is
due to mutation of specific gene that produces receptor for hypocretin, if destroyed, causes narcolepsy.
Hereditary disorder causes immune to attack/destroy hypocretinergic neurons during adolescence.
Stimulants can diminish sleep attacks, antidepressants that facilitate serotonergic/noradrenergic activity help
cataplexy, paralysis, hallucinations. Modafinil stimulant acts on hypocretinergic neurons, increased
expression of Fos, indicates that neurons activated.
REM sleep behavior disorder: no paralysi during REM, act out dreams. Neurodegenerative disorder with
some genetic component, a.w/ Parkinson, multiple system atrophy, b/c they are a-synucleinopathies that
involve inclusion of a-synuclein protein in degenratin neurons. Disorder can be caused by brain damage.
Opposite of cataplexy – instead of paralysis outside REM, no paralysis during REM.
Problems a.w/ slow-wave sleep: maladaptive behaviors such as nocturnal enuresis, somnambulism, pavor
nocturnus, esp. in children. Sleep-related eating disorder: helped by dopaminergic agonists, anxiolytic
drugs, antianxiety drugs. May be hereditary.
Functions of slow-wave sleep: only warm-blooded vertebrates show REM sleep. Essential to survival.
Dolphins sleep 4-60 seconds at a time, indicates necessary for survival. Cerebral hemispehres take turns
sleeping so one is always alert.
o Effects of sleep deprivation: does not interfere with physical exercise, no physiological stress
response, so primary role is rest/recuperation. Cognitive abilities affected. Never recover all sleep lost, higher percentage of stage 4 and REM. High metabolic rate a.w/ waking activity of brain
creates waste product of free radicals, chemicals with at least one unpaired electron. Highly reactive
oxidizing agents, bind w/ electrons from other moleceuls and damage cells through oxidative stress.
During slow-wave sleep, lowered metabolic rate permits restorative mechanisms in cells to destroy
free radicals. Prolonged sleep deprivation caused increase in free radicals and oxidative stress. Fatal
familial insomnia: inherited neuro disorder, results in damage to portions of the thalamus.
Symptoms include attention/memory deficits, confused state, loss of ANS control and endocrine
system, insomnia. First sins are fewer sleep spindles and K complexes. Slow-wave sleep disappears,
minimum REM w/o paralysis. Studies with animals need procedure to kep animals awake, yoked-
control procedure deprives one ra of sleep but forces both to exercise equal amount of time. Sleep-
deprived rats eventually died, cause still not understood, because brains appeared no normal, no
signs of inflammation, damage, stress hormones.
o Effects of exercise on sleep: brain may need slow-wave to recover from day’s activities but rest of
body does not. No changes in slow-wave/REM between active and non-active people.
o Effects of mental activity on sleep: tasks that demand alertness and mental activity increase glucose
metabolism in brain, especially in frontal lobes, where delta activity is most intense during slow-
wave sleep. Experiment shows that increased mental exercise caused increased slow-wave esp. stage
Functions of REM sleep: intense physiological activity, more pressure to go into REM during deprivation.
Rebound phenomenon: increase in REM after deprivation, suggests REM controlled by regulatory
mechanism. Highest proportion of REM seen during most active phase of brain development, might play
role in process of development – 70% for newborns, declines to 15% by adulthood. Needed in adults maybe
b/c facilitates modest changes responsbiel for learning later in life, emotional memories
consolidates/integrated, or to flush useless info. When animals deprived of REM after participating in
training, they learn task more slowly, so REM sleep dprivation retards memory formation. Learning
something enhances consequent REM sleep. Once task well-learned, REM declines to basleine levels. REM
sleep increases during exam time, found more in intellectual children and less in retarded.
Chemical control of sleep: some physio mechanism must monitor amount of sleep we need. Could be sleep-
promoting substances during wake or wakefulness promoting substances during sleep. If sleep were
controlled by chemicals in the blood, hemispheres would sleep at same time, so if it is controlled by
chemicals, they must be produced within brain and act there. Adenosine: nucleoside neuromodulator might
play role in control of sleep: active brain regions take glucose from astrocytes; metabolism of glycogen
causes increase in adenosine, which has inhibitory effects, produces increased amounts of delta activity
during next night’s sleep
Neural control of arousal:
o ACh: involved in arousal of cerebral cortex. Acetylcholingeric neurons in pons and basal forebrain
produce activation and cortical desynchrony when stimulated. Antagonists decrease EEG signs of
cortical arousal and agonists icnrase. ACh levels in striatum/hippocampus/frrtonal cortex closely
related to level of activity. Stimulation of dorsal pons activated cerebral cortex, increased release of
o NE: locus coeruleus: noradrenergic cells in pons involve din arousal/vigilance, give rise to axons
that release NE throughout brain. NE neurons in LC related to behavioral arousal; decline in firing
before/during sleep and increase during wake, falls to zero during REM, might control it. NE LC
neurons increase animal’s vigilance, control muscular activity
o Serotonin: most serotonergic neurons found in raphe nuclei in medullary/pontine regions of RF,
axons project to many parts of brain, stimulation causes locomotion/cortical arousal. PCPA drug
prevents synthesis of serotonin, reduces cortical arousal. Do not respond to external stimuli that
produce pain/stress. Facilitate continuous, automatic movements, activity decreases during orienting
response to novel stimuli. Facilitate ongoing activities, suppress sensory info processing to prevent
reactions that might disrupt ongoing activity. o Histamine: antihistamines cause drowsiness by blocking histamine h1 receptors in brain if they cross
blood-brain barrier. Histaminergic neurons located in t