Circadian Rhythms and Sleep in Humans

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.
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
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.
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.
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.
Mechanisms of the circadian rhythms include
the following:
The Suprachiasmatic nucleus.
Genes that produce certain proteins.
Melatonin levels.
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
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.
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
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.
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 phase-
advance the internal clock and can be used
as a sleep aid.
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.
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
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.
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.
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.
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.
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.
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
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.
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
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
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.
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
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
Mechanisms
The hypothalamus contains neurons that
release histamine to produce widespread
excitatory effects throughout the brain.
Anti-histamines produce sleepiness.
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.
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.
Mechanisms
(contd):
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.
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.
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
Mechanisms
Cells in the pons send messages to the
spinal cord which inhibit motor neurons that
control the bodys 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.
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, Parkinsons 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
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.
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.
Mechanisms
(Insomnia contd)
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.
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.
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
Parkinsons.
Associated with damage to the pons
(inhibit the spinal neurons that control large
muscle movements).
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.
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.
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
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.
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.
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.
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
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.
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.
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.
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.
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.
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.
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.
Activity is high in the inferior part of the
parietal cortex, an area important for visual-
spatial 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.
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.

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Chapter 9

Wakefulness and Sleep

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