Chapter 9

Report
Chapter 9
Wakefulness and Sleep
Rhythms of Waking and Sleep
• Animals generate endogenous 24 hour cycles
of wakefulness and sleep.
• Some animals generate endogenous
circannual rhythms, internal mechanisms that
operate on an annual or yearly cycle.
– Example: Birds migratory patterns, animals
storing food for the winter.
Rhythms of Waking and Sleep
• All animals produce endogenous circadian
rhythms, internal mechanisms that operate on
an approximately 24 hour cycle.
– Regulates the sleep/ wake cycle.
– Also regulates the frequency of eating and
drinking, body temperature, secretion of
hormones, volume of urination, and
sensitivity to drugs.
Fig. 9-2, p. 267
Rhythms of Waking and Sleep
Circadian rhythms:
• Remains consistent despite lack of
environmental cues indicating the time of day
• Can differ between people and lead to
different patterns of wakefulness and
alertness.
• Change as a function of age.
– Example: sleep patterns from childhood to
late adulthood.
Rhythms of Waking and Sleep
• Experiments designed to determine the
length of the circadian rhythm place subjects
in environments with no cues to time of day.
• Results depend upon the amount of light to
which subjects are artificially exposed.
– Rhythms run faster in bright light conditions
and subjects have trouble sleeping.
– In constant darkness, people have difficulty
waking.
Rhythms of Waking and Sleep
• Human circadian clock generates a rhythm
slightly longer than 24 hours when it has no
external cue to set it.
• Most people can adjust to 23- or 25- hour day
but not to a 22- or 28- hour day.
• Bright light late in the day can lengthen the
circadian rhythm.
Rhythms of Waking and Sleep
• Mechanisms of the circadian rhythms include
the following:
– The Suprachiasmatic nucleus.
– Genes that produce certain proteins.
– Melatonin levels.
Rhythms of Waking and Sleep
• The suprachiasmatic nucleus (SCN) is part of
the hypothalamus and the main control center
of the circadian rhythms of sleep and
temperature.
– Located above the optic chiasm.
– Damage to the SCN results in less
consistent body rhythms that are no longer
synchronized to environmental patterns of
light and dark.
Fig. 9-4, p. 269
Rhythms of Waking and Sleep
• The SCN is genetically controlled and
independently generates the circadian
rhythms.
• Single cell extracted from the SCN and raised
in tissue culture continues to produce action
potential in a rhythmic pattern.
• Various cells communicate with each other to
sharpen the circadian rhythm.
Rhythms of Waking and Sleep
•
Two types of genes are responsible for
generating the circadian rhythm.
1. Period - produce proteins called Per.
2. Timeless - produce proteins called Tim.
• Per and Tim proteins increase the activity of
certain kinds of neurons in the SCN that
regulate sleep and waking.
• Mutations in the Per gene result in odd
circadian rhythms.
Fig. 9-5, p. 270
Rhythms of Waking and Sleep
• The SCN regulates waking and sleeping by
controlling activity levels in other areas of the
brain.
• The SCN regulates the pineal gland, an
endocrine gland located posterior to the
thalamus.
• The pineal gland secretes melatonin, a
hormone that increases sleepiness.
Rhythms of Waking and Sleep
• Melatonin secretion usually begins 2 to 3
hours before bedtime.
• Melatonin feeds back to reset the biological
clock through its effects on receptors in the
SCN.
• Melatonin taken in the afternoon can phaseadvance the internal clock and can be used
as a sleep aid.
Rhythms of Waking and Sleep
• The purpose of the circadian rhythm is to
keep our internal workings in phase with the
outside world.
• Light is critical for periodically resetting our
circadian rhythms.
• A zeitgeber is a term used to describe any
stimulus that resets the circadian rhythms.
• Exercise, noise, meals, and temperature are
others zeitgebers.
Rhythms of Waking and Sleep
• Jet lag refers to the disruption of the circadian
rhythms due to crossing time zones.
– Stems from a mismatch of the internal
circadian clock and external time.
• Characterized by sleepiness during the day,
sleeplessness at night, and impaired
concentration.
• Traveling west “phase-delays” our circadian
rhythms.
• Traveling east “phase-advances” our
circadian rhythms.
Fig. 9-6, p. 272
Rhythms of Waking and Sleep
• Light resets the SCN via a small branch of the
optic nerve known as the retinohypothalamic
path.
– Travels directly from the retina to the SCN.
• The retinohypothalamic path comes from a
special population of ganglion cells that have
their own photopigment called melanopsin.
– The cells respond directly to light and do
not require any input from the rods or
cones.
Stages of Sleep And Brain
Mechanisms
• Sleep is a specialized state that serves a
variety of important functions including:
– conservation of energy.
– repair and restoration.
– learning and memory consolidation.
Stages of Sleep And Brain
Mechanisms
• The electroencephalograph (EEG) allowed
researchers to discover that there are various
stages of sleep.
• Over the course of about 90 minutes:
– a sleeper goes through sleep stages 1, 2,
3, and 4
– then returns through the stages 3 and 2 to
a stage called REM.
Stages of Sleep And Brain
Mechanisms
• Alpha waves are present when one begins a
state of relaxation.
• Stage 1 sleep is when sleep has just begun.
– the EEG is dominated by irregular, jagged,
low voltage waves.
– brain activity begins to decline.
Stages of Sleep And Brain
Mechanisms
• Stage 2 sleep is characterized by the
presence of:
– Sleep spindles - 12- to 14-Hz waves during
a burst that lasts at least half a second.
– K-complexes - a sharp high-amplitude
negative wave followed by a smaller,
slower positive wave.
Stages of Sleep And Brain
Mechanisms
• Stage 3 and stage 4 together constitute slow
wave sleep (SWS) and is characterized by:
– EEG recording of slow, large amplitude
wave.
– Slowing of heart rate, breathing rate, and
brain activity.
– Highly synchronized neuronal activity.
Stages of Sleep And Brain
Mechanisms
• Rapid eye movement sleep (REM) are
periods characterized by rapid eye
movements during sleep.
• Also known as “paradoxical sleep” because it
is deep sleep in some ways, but light sleep in
other ways.
• EEG waves are irregular, low-voltage and
fast.
• Postural muscles of the body are more
relaxed than other stages.
Fig. 9-9, p. 276
Stages of Sleep And Brain
Mechanisms
• Stages other than REM are referred to as
non-REM sleep (NREM).
• When one falls asleep, they progress through
stages 1, 2, 3, and 4 in sequential order.
• After about an hour, the person begins to
cycle back through the stages from stage 4 to
stages 3 and 2 and than REM.
• The sequence repeats with each cycle lasting
approximately 90 minutes.
Stages of Sleep And Brain
Mechanisms
• Stage 3 and 4 sleep predominate early in the
night.
– The length of stages 3 and 4 decrease as
the night progresses.
• REM sleep is predominant later in the night.
– Length of the REM stages increases as the
night progresses.
• REM is strongly associated with dreaming,
but people also report dreaming in other
stages of sleep.
Fig. 9-10, p. 277
Stages of Sleep And Brain
Mechanisms
• Various brain mechanisms are associated
with wakefulness and arousal.
• The reticular formation is a part of the
midbrain that extends from the medulla to the
forebrain and is responsible for arousal.
Table 9-1, p. 280
Stages of Sleep And Brain
Mechanisms
• The pontomesencephalon is a part of the
midbrain that contributes to cortical arousal.
– Axons extend to the thalamus and basal
forebrain which release acetylcholine and
glutamate
– produce excitatory effects to widespread
areas of the cortex.
• Stimulation of the pontomesencephalon
awakens sleeping individuals and increases
alertness in those already awake.
Stages of Sleep And Brain
Mechanisms
• The locus coeruleus is small structure in the
pons whose axons release norepinephrine to
arouse various areas of the cortex and
increase wakefulness.
– Usually dormant while asleep.
Fig. 9-11, p. 279
Stages of Sleep And Brain
Mechanisms
• The basal forebrain is an area anterior and
dorsal to the hypothalamus containing cells
that extend throughout the thalamus and
cerebral cortex.
• Cells of the basal forebrain release the
inhibitory neurotransmitter GABA.
• Inhibition provided by GABA is essential for
sleep.
• Other axons from the basal forebrain release
acetylcholine which is excitatory and
increases arousal.
Fig. 9-12, p. 280
Stages of Sleep And Brain
Mechanisms
• The hypothalamus contains neurons that
release “histamine” to produce widespread
excitatory effects throughout the brain.
– Anti-histamines produce sleepiness.
Stages of Sleep And Brain
Mechanisms
• Orexin is a peptide neurotransmitter released
in a pathway from the lateral nucleus of the
hypothalamus highly responsible for the
ability to stay awake.
– Stimulates acetylcholine-releasing cells in
the forebrain and brain stem to increase
wakefulness and arousal.
Stages of Sleep And Brain
Mechanisms
•
Decreased arousal required for sleep is
accomplished via the following ways:
1. Decreasing the temperature of the brain
and the body.
2. Decreasing stimulation by finding a quiet
environment.
3. Accumulation of adenosine in the brain to
inhibit the basal forebrain cells
responsible for arousal.
– Caffeine blocks adenosine receptors.
Stages of Sleep And Brain
Mechanisms
(cont’d):
4. Accumulation of prostaglandins that
accumulate in the body throughout the day
to induce sleep.
– Prostaglandins stimulate clusters of
neurons that inhibit the hypothalamic
cells responsible for increased arousal.
Stages of Sleep And Brain
Mechanisms
• During REM sleep:
– Activity increases in the pons (triggers the
onset of REM sleep), limbic system,
parietal cortex and temporal cortex.
– Activity decreases in the primary visual
cortex, the motor cortex, and the
dorsolateral prefrontal cortex.
Stages of Sleep And Brain
Mechanisms
• REM sleep is also associated with a
distinctive pattern of high-amplitude electrical
potentials known as PGO waves.
• Waves of neural activity are detected first in
the pons and then in the lateral geniculate of
the hypothalamus, and then the occipital
cortex.
• REM deprivation results in high density of
PGO waves when allowed to sleep normally.
Fig. 9-13, p. 281
Stages of Sleep And Brain
Mechanisms
• Cells in the pons send messages to the
spinal cord which inhibit motor neurons that
control the body’s large muscles.
– Prevents motor movement during REM
sleep.
• REM is also regulated by serotonin and
acetylcholine.
– Drugs that stimulate Ach receptors quickly
move people to REM.
– Serotonin interrupts or shortens REM.
Stages of Sleep And Brain
Mechanisms
• Insomnia is a sleep disorder associated with
inability to fall asleep or stay asleep.
– Results in inadequate sleep.
– Caused by a number of factors including
noise, stress, pain medication.
– Can also be the result of disorders such as
epilepsy, Parkinson’s disease, depression,
anxiety or other psychiatric conditions.
– Dependence on sleeping pills and shifts in
the circadian rhythms can also result in
insomnia.
Fig. 9-15, p. 282
Stages of Sleep And Brain
Mechanisms
• Sleep apnea is a sleep disorder characterized
by the inability to breathe while sleeping for a
prolonged period of time.
• Consequences include sleepiness during the
day, impaired attention, depression, and
sometimes heart problems.
• Cognitive impairment can result from loss of
neurons due to insufficient oxygen levels.
• Causes include, genetics, hormones, old age,
and deterioration of the brain mechanisms
that control breathing and obesity.
Stages of Sleep And Brain
Mechanisms
• Narcolepsy is a sleep disorder characterized
by frequent periods of sleepiness.
• Four main symptoms include:
– Gradual or sudden attack of sleepiness.
– Occasional cataplexy - muscle weakness
triggered by strong emotions.
– Sleep paralysis- inability to move while
asleep or waking up.
– Hypnagogic hallucinations- dreamlike
experiences the person has difficulty
distinguishing from reality.
Stages of Sleep And Brain
Mechanisms
(Insomnia cont’d)
• Seems to run in families although no gene
has been identified.
• Caused by lack of hypothalamic cells that
produce and release orexin.
• Primary treatment is with stimulant drugs
which increase wakefulness by enhancing
dopamine and norepinephrine activity.
Stages of Sleep And Brain
Mechanisms
• Periodic limb movement disorder is the
repeated involuntary movement of the legs
and arms while sleeping.
– Legs kick once every 20 to 30 seconds for
periods of minutes to hours.
– Usually occurs during NREM sleep.
Stages of Sleep And Brain
Mechanisms
• REM behavior disorder is associated with
vigorous movement during REM sleep.
– Usually associated with acting out dreams.
– Occurs mostly in the elderly and in older
men with brain diseases such as
Parkinson’s.
– Associated with damage to the pons
(inhibit the spinal neurons that control large
muscle movements).
Stages of Sleep And Brain
Mechanisms
• “Night terrors” are experiences of intense
anxiety from which a person awakens
screaming in terror.
– Usually occurs in NREM sleep.
• “Sleep talking” occurs during both REM and
NREM sleep.
• “Sleepwalking” runs in families, mostly occurs
in young children, and occurs mostly in stage
3 or 4 sleep.
Why Sleep? Why REM? Why Dreams?
• Functions of sleep include:
– Energy conservation.
– Restoration of the brain and body.
– Memory consolidation.
Why Sleep? Why REM? Why Dreams?
• The original function of sleep was to probably
conserve energy.
• Conservation of energy is accomplished via:
– Decrease in body temperature of about 1-2
Celsius degrees in mammals.
– Decrease in muscle activity.
Why Sleep? Why REM? Why Dreams?
• Animals also increase their sleep time during
food shortages.
– sleep is analogous to the hibernation of
animals.
• Animals sleep habits and are influenced by
particular aspects of their life including:
– how many hours they spend each day
devoted to looking for food.
– Safety from predators while they sleep
• Examples: Sleep patterns of dolphins,
migratory birds, and swifts.
Fig. 9-17, p. 287
Why Sleep? Why REM? Why Dreams?
• Sleep enables restorative processes in the
brain to occur.
– Proteins are rebuilt.
– Energy supplies are replenished.
• Moderate sleep deprivation results in
impaired concentration, irritability,
hallucinations, tremors, unpleasent mood,
and decreased responses of the immune
system.
Why Sleep? Why REM? Why Dreams?
• People vary in their need for sleep.
– Most sleep about 8 hours.
• Prolonged sleep deprivation in laboratory
animals results in:
– Increased metabolic rate, appetite and
body temperature.
– Immune system failure and decrease in
brain activity.
Why Sleep? Why REM? Why Dreams?
• Sleep also plays an important role in
enhancing learning and strengthening
memory.
– Performance on a newly learned task is
often better the next day if adequate sleep
is achieved during the night.
• Increased brain activity occurs in the area of
the brain activated by a newly learned task
while one is asleep.
– Activity also correlates with improvement in
activity seen the following day.
Why Sleep? Why REM? Why Dreams?
• Humans spend one-third of their life asleep.
• One-fifth of sleep time is spent in REM.
• Species vary in amount of sleep time spent in
REM.
– Percentage of REM sleep is positively
correlated with the total amount of sleep in
most animals.
• Among humans, those who get the most
sleep have the highest percentage of REM.
Fig. 9-18, p. 289
Why Sleep? Why REM? Why Dreams?
• REM deprivation results in the following:
– Increased attempts of the brain/ body for
REM sleep throughout the night.
– Increased time spent in REM when no
longer REM deprived.
• Subjects deprived of REM for 4 to 7
nights increased REM by 50% when no
longer REM deprived.
Why Sleep? Why REM? Why Dreams?
• Research is inconclusive regarding the exact
functions of REM.
• During REM:
– The brain may discard useless connections
– Learned motor skills may be consolidated.
• Maurice (1998) suggests the function of REM
is simply to shake the eyeballs back and forth
to provide sufficient oxygen to the corneas.
Why Sleep? Why REM? Why Dreams?
•
Biological research on dreaming is
complicated by the fact that subjects can not
often accurately remember what was
dreamt.
• Two biological theories of dreaming include:
1. The activation-synthesis hypothesis.
2. The clinico-anatomical hypothesis.
Why Sleep? Why REM? Why Dreams?
• The activation-synthesis hypothesis suggests
dreams begin with spontaneous activity in the
pons which activates many parts of the
cortex.
– The cortex synthesizes a story from the
pattern of activation.
– Normal sensory information cannot
compete with the self-generated
stimulation and hallucinations result.
Why Sleep? Why REM? Why Dreams?
• Input from the pons activates the amygdala
giving the dream an emotional content.
• Because much of the prefrontal cortex is
inactive during PGO waves, memory of
dreams is weak.
– Also explains sudden scene changes that
occur in dreams.
Why Sleep? Why REM? Why Dreams?
• The clinico-anatomical hypothesis places less
emphasis on the pons, PGO waves, or even
REM sleep.
– Suggests that dreams are similar to
thinking, just under unusual circumstances.
• Similar to the activation synthesis hypothesis
in that dreams begin with arousing stimuli that
are generated within the brain.
– Stimulation is combined with recent
memories and any information the brain is
receiving from the senses.
Why Sleep? Why REM? Why Dreams?
• Since the brain is getting little information
from the sense organs, images are generated
without constraints or interference.
• Arousal can not lead to action as the primary
motor cortex and the motor neurons of the
spinal cord are suppressed.
• Activity in the prefrontal cortex is suppressed
which impairs working memory during
dreaming.
Why Sleep? Why REM? Why Dreams?
• Activity is high in the inferior part of the
parietal cortex, an area important for visualspatial perception.
– Patients with damage report problems with
binding body sensations with vision and
have no dreams.
– Activity is also high in areas outside of V1,
accounting for the visual imagery of
dreams.
Why Sleep? Why REM? Why Dreams?
• Activity is high in the hypothalamus and
amygdala which accounts for the emotional
and motivational content of dreams.
• Either internal or external stimulation
activates parts of the parietal, occipital, and
temporal cortex.
• Lack of sensory input from V1 and no
criticism from the prefrontal cortex creates the
hallucinatory perceptions.

similar documents