SLEEP & CIRCADIAN
RHYTHMS
Images in these slides were obtained from the following sources:
Carlson, Physiology of Behavior, 9th edition (2007) Allyn and Bacon
Rosenzweig, Leiman and Breedlove, Biological Psychology (2001) Sinaur Associates, Inc
SLEEP PHYSIOLOGY

PHYSIOLOGICAL MEASURES
 Electroencephalogram
 brain
waves from scalp surface
 Electrooculogram
 eye
(EEG)
(EOG)
movements
 Electromyogram
 muscle
tone
(EMG)
SLEEP PHYSIOLOGY
 EEG
Waves (wakefulness)
 beta waves
 Irregular
low amp., high freq. waves (13-30 Hz)
 indicative of alert and vigilant activity
 alpha
waves
 regular
medium freq. waves (8-12 Hz)
 resting quietly, but awake
SLEEP PHYSIOLOGY

SLEEP STAGES
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Stage 1: alpha and theta
waves (initial)
Stage 2: K complexes, sleep
spindles
Stage 3: 20-50% delta
(SWS)
Stage 4: > 50% delta (SWS)
REM (emergent stage 1)
SLEEP PHYSIOLOGY
 REM
SLEEP
increased cerebral activity, erratic EEG (beta and
theta waves)
 rapid eye movements
 loss of core muscle tone (paralysis)
 autonomic arousal (elevated hr, bp, and respiration)
 narrative dreams with much visual imagery
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initially referred to as “PARADOXICAL
SLEEP”
SWS VS. REM SLEEP
SLEEP CYCLES
SLEEP PATTERNS
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Percent of SWS vs. REM changes with age
Young Adult sleep patterns consist of:
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7-8 hours of 90-110 min. repeating cycles
45-50% of total sleep is stage 2
20% of total sleep is REM sleep
More SWS early in night
Progressive lengthening of REM periods
LIFE SPAN CHANGES
IN SLEEP
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Daily sleep rhythms begin ~ 16 weeks.
Greater % REM in infants and children.
REM component decreases with age.
Total sleep time decreases with age.
Elderly frequently experience insomnia and
decreased SWS.
LIFE SPAN CHANGES
IN SLEEP
SLEEP DISORDERS
 INSOMNIA
affects ~25% of population
occasionally, ~9% regularly
 No single definition
 Insomnia is symptom, not a disease
 multiple causes, often iatrogenic

 tolerance
to sedative-hypnotic drugs
 frequent symptom of depression
 Other causes: sleep apnea, nocturnal
myoclonus, restless legs (PLMD)
SLEEP DISORDERS
 Sleep-onset
 difficulties
 Sleep
insomnia
falling asleep
maintenance insomnia
 frequent
awakenings, may be associated
with SLEEP APNEA (difficulty breathing
while asleep)
SLEEP DISORDERS
 NARCOLEPSY

Characteristic Symptoms:
Sleep Attack (5-30 minutes)
 Cataplexy
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frequently brought on by intense emotions
Immediate REM at sleep onset
Sleep Paralysis
 Hypnogogic Hallucinations
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SLEEP DISORDERS
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NARCOLEPSY
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Heritability and Hypocretin (Orexin)
Genetic models in dogs
 increased ACh receptors in pons
 amygdala and forebrain degeneration
 canarc gene (Hypocretin 2 receptors)
Hypocretin gene knockout mouse model
CSF analysis in human narcoleptic patients show
diminished hypocretin levels.
SLEEP DISORDERS

REM SLEEP BEHAVIOR DISORDER
Characterized by failure to exhibit muscle paralysis
during REM sleep
 Appears to be neurodegenerative disorder with some
possible genetic component
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Often associated with other neurodegenerative disorders,
such as Parkinson’s disease
Usually treated with clonazepam, a benzodiazepine
SLEEP DISORDERS

COMMON CHILDHOOD SLEEP
DISORDERS ASSOSCIATED WITH
SLOW WAVE SLEEP
 Pavor
Nocturnus (night terrors)
 Somnambulism (sleep walking)
 Nocturnal Enuresis (bed wetting)
SLEEP FUNCTIONS
(Why do we sleep?)

Restorative Functions
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growth and repair
Adaptive Functions
predator avoidance
 energy conservation
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Cognitive Functions
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learning, unlearning, reorganization
COMPARATIVE STUDIES OF
SLEEP
SLEEP IN MARINE
MAMMALS
SLEEP DEPRIVATION
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Early reports of bizarre or psychotic behavior
Wide individual variability (personality and
age factors)
Most common effects of sleep deprivation:
increased irritability
 decreased concentration
 Confusion/disorientation
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SLEEP DEPRIVATION
IN HUMANS
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Performance on brief tasks is unimpaired.
Performance on tasks that involve high
motivation are generally not impaired.
Sleep Recovery (Randy Gardner story)
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11 days (264 hours) sleep deprivation
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1st night, ~ 15 hours; stage 4 increased at expense of stage 2
2nd night, ~10 hours; greatest REM recovery
Percentages of sleep recovery not equivalent across all stages:
7% of stages 1 and 2, 68% SWS, 53% REM sleep “made up”
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SLEEP DEPRIVATION IN
NONHUMANS
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It is difficult to tease apart effects of sleep
deprivation versus stressful effects of the procedure.

Rechtschaffen and Bergmann, 1995
Carousel apparatus with yoked controls
 Experimental animals died within days, while
controls remained relatively healthy.
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EFFECTS OF ACTIVITIES ON
SLEEP

Effects of Exercise on Sleep
Does the brain recover from day time physical
exertion?
 Little compelling evidence: People who spend much
of their time resting in bed do not sleep less
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Effects of Mental Activity on Sleep
Does the brain recover from day time mental
exertion?
 Some studies have shown that extensive mental
activities are followed by normal sleep duration, but
increased SWS.
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FUNCTIONS OF REM SLEEP
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Theories that REM sleep is required for normal
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Interesting links between REM sleep and
depression
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Mental health
Motivation
Cognitive processing
REM deprivation has antidepressant effects
Most antidepressant drugs also reduce REM sleep.
There’s considerable research on links between
REM sleep and learning/memory.
REM SLEEP DEPRIVATION
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Following REM deprivation, there is a
compensatory increase in REM sleep, which
seems to suggest REM sleep is a necessary brain
function.
Some evidence that REM deprivation can
produce cognitive/memory deficits.
Some evidence that REM sleep increases
following new learning.
NEURAL MECHANISMS
OF SLEEP
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Basal Forebrain
Brain Stem Reticular Formation
Raphe nucleus (midbrain)
Locus Coeruleus (pons)
Lateral hypothalamus
NEURAL MECHANISMS
OF SLEEP

Sleep is an active state mediated by at
least three neural systems
 Forebrain:
generates SWS
 Reticular Formation: Wakes Forebrain
 Pons: Triggers REM sleep
NEURAL MECHANISMS
OF SLEEP
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Bremer (1935)
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Moruzzi and Magoun
(1949)
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Encephale isole
Cerveau isole
Reticular formation
Jouvet (1967)
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Raphe system
NEURAL MECHANISMS
OF SLEEP
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BASAL FOREBRAIN
ventral frontal lobe, anterior hypothalamus
 lesions abolish SWS
 electrical or heat stimulation can induce
SWS activity
 These neurons are active at sleep onset
 Inhibited by NE stimulation
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NEURAL MECHANISMS
OF SLEEP
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RETICULAR
FORMATION
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central core of brain stem
diffuse group of cells extending
from medulla to thalamus
electrical stimulation produces
arousal, awakens a sleeping
animal
lesions produce persistent sleep
NEURAL MECHANISMS
OF SLEEP
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RAPHE NUCLEI
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A system of serotonergic
neurons along midline of brain
stem.
Lesions to Raphe nuclei produce
insomnia.
PCPA inhibits 5-HT synthesis
and reduces sleep, whereas 5-HT
agonists promote sleep
NEURAL MECHANISMS
OF SLEEP
 PONS
crucial for REM sleep components
 lesions ventral to Locus Coeruleus abolish REM
sleep
 electrical or pharmacological stimulation (ACh
agonists) can induce or prolong REM sleep
 small lesions ventral to LC selectively abolish
REM muscle atonia
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NEUROTRANSMITTERS AND
SLEEP
CIRCADIAN RHYTHMS
 DEFINITION
 24
hr. endogenous cycles
 EXAMPLES
 sleep/wake
cycle
 body temperature
 hormone secretion
 drug sensitivity
LABORATORY STUDIES OF
CIRCADIAN RHYTHMS
CIRCADIAN RHYTHMS

TERMINOLOGY
 Free
Running Period
 Entrainment
 Zeitgeber
 Phase Shifts
 phase
advances: acceleration of
circadian rhythm
 phase delays: deceleration of
circadian rhythm
CIRCADIAN RHYTHMS

Circadian Timing Mechanisms
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Internal desynchronization of S-W cycle and body
temp. cycle suggest separate timing mechanisms.
Common Examples of Phase Shifts
Jet Lag results from phase shifts in circadian
rhythms as a result of traveling across time zones.
 Shift workers often forced to adjust S-W cycle. Such
disruptions may affect health and productivity.
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NEURAL MECHANISMS
OF CIRCADIAN RHYTHMS
SUPRACHIASMATIC NUCLEUS
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Experimental Research on SCN involvement
in circadian rhythms
Large lesions of hypothalamus disrupt circadian
cycles of activity in rats. (Richter, 1967)
 Lesions specific to SCN disrupt periodicity of
sleep/wake cycle
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 SCN
displays circadian cycles of electrical,
metabolic, and biochemical activity.
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Fetal tissue transplants in hamsters
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Fetal tissue from 20 hour donor implanted in 25 hour
recipient after SCN lesion.
Recipient becomes entrained to 20 hour cycle
SUPRACHIASMATIC NUCLEUS