PY460:
Physiological
Psychology
Chapter 9: Rhythms of Wakefulness & Sleep
Rhythms of Waking & Sleeping
Stages of Sleep and Brain Mechanisms
Why Sleep? Why REM? Why Dreams?
Slide 2: Natural Cycles of Biological Activity
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[Clip: The Brain- Sleep & Circadian Rhythms]
Curt Richter (1920’s)- biological beings have
naturally occurring biological cycles largely
independent of the outside world.
Challenge to behaviorism in the mid-1900’s
 why?
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Endogeneous cycles- of evolutionary value
anticipation of upcoming conditions
 migration
 storage
mating
“migratory restlessness” in willow warblers
 occurs despite lack of environmental cues (light)
Slide 3: Specific Endogenous Cycles
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Endogenous Circannual Rhythms
internal cycles that prepares animal for
seasonal changes
 storage of fats, hibernation, humans???
Endogenous Circadian Rhythms
internal cycles (rhythms) that prepares animal
for changes that last about a day.
Most Familiar Rhythm? Sleep & Wakefulness!
Others include: core body temperature,
frequencyt of eating & drinking, hormonal
secretion, chemical sensitivities (drugs).
Slide 4: Zeitgebers: Keeping Rhythms in Synchrony
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All rhythms typically stay in synchrony suggesting
a “master biological clock” exists (more on this in a
bit).
We know that our free running rhythms are often
greater than 24 hrs. (24.25- 24.75 hrs.).
Why don’t we (and other animals) get “off-pace”
with the 24 hours daily cycle?
AH…LIGHT the primary Zeitgeber (say like a
German)- resets the master clock.
other “time keepers”- noises, meals,
temperature variations
Slide 5: Mammoth Cave etc.- Altering the Biological Clock?
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What is humans traveled to a planet with a different daily
cycle (say 20-30 hrs)? How would we adjust?
Mammoth Cave study (1963).
 A month in a cave (temperature and light controlled).
 28 hr days, (9 hrs sleep). What would happen to their cycle?
 Findings: Continued maintenance of the 24 hour clock…
subjects could force themselves into the schedule but, bodies
maintained original rhythms.
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Study 2: 12 volunteers in a cave… clock varied between 2422 hours..
At 23 hrs most subjects adjusted, only 1 @ 22 hrs.
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Bottom Line- significant changes in daily rhythms very
difficult to make
Slide 6: Disturbing the Biological Clock
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Our free running clock runs longer than 24 hrs, but our days
are 24 hrs… daily readjustment keeps us in sync...
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What would changes might cause de-synchrony
between biological clock & hourly clock?
WEEKENDS (No.1)-Fewer time constraints… Often follow bioclock--Go to bed later, sleep in…get up.. Reset clock.. Go to
bed later than before.. Get up little later.. Reset clock-by Monday, bioclock hours behind the hourly clock
SHIFT WORK-- night shifts, or irregular pattern in
schedule lead to irregular sleeping patterns, temperature
often maintain daily pattern, health & safety issues.
Particularly bright light somewhat effective in
competing with day time light
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Slide 7: More Disturbances in the Bioclock
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JET LAG- rhythm disturbance caused by
crossing times zones..
Traveling west (PA to LA) (stay up later, sleep in… gain
hours )(27 hrs… tend to be ok-- more natural to be
awake a little later.. Sleep in)
Traveling East (LA to PA) (lose hours).
0
2
12 pm
local
Change
8
Wake
7am
local
To Bed
10 pm
local
LA to PA
Hourly
Arrive
+ 6hrs
Depart
9am
local
Wake
7 am
local
PA to LA
Hourly clock
18
hrs
27
+3
12 hrs
21
-3
8
0
2
6 pm
local
Slide 8: Suprachiasmatic Nucleus- the bioclock
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Suprachiasmatic Nucleus- area in the hypothalamus,
just above the optic chiasm (nerve).
Rentinohypothalamic pathway
 Autorhythmic quality may drive circadian rhythms.
Biological clock stops if damaged or Optic Nerve projecting to
SCN is damaged
Extremely sensitive to light (even in blind moles!)
 SCN reset to light
– Biochemical action unclear.. Protein production?
Slide 9: SCN & Melatonin
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Melatonin- hormone important in regulating
sleepiness & wakefulness
secreted near the end of a waking cycle.. A few hours before
typical bed time.
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Pineal Gland- secretes melatonin release at the
command of SCN.
Taking melatonin supplements (.5 mg) in the afternoon--->
phase-advances circadian rhythm (jet lag?)
Taking melatonin in morning phase-delays circadian rhythm
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A note of warning-- little extended research in area.
Slide 10: The Brain During Sleep (NREM Sleep only)
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EEG- increased wave size= greater synchrony
between two close sites on cortex.
 Provides an objective measure of sleep and wakefulness
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Stages of Sleep- characterized by a type of wave
Awake/Relaxed- Alpha Waves, Beta Waves
Stage 1: freq. irregular, jagged waves (Theta)
Stage 2: Sleep Spindles (12-14hz) & K-complexes
K-complexes evoke by sudden stimuli (noise
etc)
Stage 3 & 4: Slow wave sleep (SWS) (2hz waves)
» big slow waves (delta) indicating high synchrony
» reduced sensory input to cortex… “less noise”
» see wave and stone analogy (p. 254)
Slide 11: Synchrony & EEG
Choose the stage &
name the characteristics
• Big slow 1/2 sec waves;
highly synchronous action
• Alpha & beta waves
(smaller amplitude) regular
and choppy respectively
• sleep spindles & kcomplexes frequent here
Slide 12: REM Sleep/Paradoxical Sleep
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Michel Jouvet, Kleitman & Aserinsky- scientists
notice that during certain intervals of sleep
high levels of brain activity (almost looked awake)
no bodily movement though, in fact most relaxed state of
postural muscles
rapid eye movement in humans
increased “genital activity”
called it “paradoxical” and “REM” sleep, respectively.
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REM sleep-- low voltage, irregular waves
suggestive of considerable brain activity
Slide 13: Cycling through the stages
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Progression through
the stages @ night.
Stage 3 to 4 longest
early on
progressive
lengthening of REM
toward the final hours
REM strongly
associated with
dreaming.. But
apparently not the
only dream stage
Slide 14: Brain Structures in Wakefulness & Arousal
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The Reticular Formation- structures whose length
extends from the spinal cord up to the forebrain..
Widely connected to the sensory systems
» may easily respond to slightest sensory impulse
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Spontaneous pulsing activity regulating arousal even with
little external stimuli
Cutting through the midbrain immediately reduces arousa
Pontomesencephalon-
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Locus Coeruleus- emits arousing bursts to meaningful
events such as reinforcement/arousal and may assist in
memory of important events.
Inactive during sleep-->little memory??
Slide 15: “Arousing Brain Structures” continues
Basal Forebrain (anterior and dorsal to hypothalamus)
Damage leads to decreased arousal, impaired learning
& attention
most damaged by degradation of Alzheimer’s
Acetylcholine- an arousing neurotransmitter in BF
GETTING TO SLEEP- Inhibiting Arousal Systems
 Adenosine (declines during sleep) - a neuromodulator that
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accumulates over the course of the day and blocks ACh.
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Caffeine- blocks Adenosine--> incr. Arousal (ACh)
interferes the whole day… even a morning cup of “Joe”.
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Prostaglandins- (decline during sleep)
Slide 16: Brain Functions in REM Sleep: PGO Waves
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The first indication of approaching REM sleep are
short burst from the Pons, lateral Geniculate, &
Occipital Cortex (PGO waves) (see text figure 9.12)
LG and OC critical for vision processes-- REM primarily a
visual phenomenon?
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First part of REM--- LG / OC manipulation
Latter-- more thalamus than just LG and the
cerebral cortex… becomes a less visual
phenomena.
Pons-- pulses related to sleep paralysis
damage to Pons cell to the spinal cord leads to
disinhibtion of behavior during sleep (fig 9.13).
Slide 17: Abnormalities of Sleep/Insomnias
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Causes: many
 caffeine, drugs, stress,
temperatures
Onset insomnia
Maintenance Insomnia
Termination Insomnia
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Irregularities in biorhythms
phase delayed
» onset an issue
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phase advanced
» termination an
issue
Slide 18: Other Abnormalities of Sleep
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Sleep Apnea- inability to breath during sleep-- cuts sleep times
in half in worst cases…. Linked to obesity
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SIDS
Narcolepsy- intrusion of REM into “wakeful”states
 sudden sleepiness during day
 cataplexy- muslce weakness while awake
 frequent sleep paralysis even during “twilight” states
 Hypnogogic hallucinations on early onset.
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PLMD- decr sleep paralysis (Pons?)
REM Bhvr Disorder-act out dreams (damage to pons & midbrain)
Night Terrors-screaming in terror during NREM sleep
Talking in Sleep (REM or NREM sleep)
Sleepwalking- strong genetic component
» awakening sleep walkers
Slide 19: What is sleep for? Theories on Function
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Repair & Restoration Theory- Sleep evolved to
assist the body in repairing itself after the exertions
of the day.
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Going without sleep-- psychological effects (what are
they?)
Physiological f/x: increased body temp, metabolic rate,
appetite; decreased immune response.
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Evolutionary Theory of Sleep- a form of minihibernation… we sleep when food is scarce and
danger is greater.. Conserves energy when we
can’t replenish it easily or safely.
Temp decreases, metabolism decreases
Carnivores/Herbivores sleep patterns
Slide 20: The Function of REM- What is it good for?
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Abundance of REM during early childhood
» neuronal connections?? (see fig 9.17, pg276)
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REM varies from person to person..
 It has been suggested we could go without it (Horne, 1988).
So what if we do go without?? (Dement, 1960)
Dement woke subject for a week every time went into REM
stage
 effects: decreased time to REM sleep.. Up to an average of
26 times of waking per night by 7 day up from 12 on the first
 effects: increased anxiety, decreased concentration,
personality change, increased appetite/weight gain.
Cat research
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other hypotheses on roles of REM sleep
 REM assists in memory formation
 Increased oxygen delivery to retina’s
Slide 21: A Biological Perspective on Dreaming
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Freud- Dreaming symbolic of unconscious wishes (“wish fulfillment”)
Activation-synthesis hypothesis- various external stimuli
activate structures in the brain and are synthesized by
the brain into a “story”.
 Is this sensible to you… how have external stimuli been
incorporated into your dreams?
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Another version.. The brain is active during REM sleep but
starved for stimuli.. In this absence---> borrows aspects from
memory to construct a story.
Flying sensations (vesitbular pulses)
Slow movement dreams (postural muscles frozen)
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Clinico-Anatomical Hypothesis
 Dreams begin with arousing stimuli from the brain’s own
motivations, memories, and arousal
 Does not compete with visual input or censorship by
prefrontal cortex