chapter 9 wakefulness and sleep. rhythms of waking and sleep animals generate endogenous 24 hour...

Chapter 9Wakefulness 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.


• 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.


• 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.


• 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.


• 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.


• 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 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.


• 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


• 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


• 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.


• 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


• 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


• The hypothalamus contains neurons that release “histamine” to produce widespread excitatory effects throughout the brain.– Anti-histamines produce sleepiness.


• 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.


• 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.


(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.


• 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.


• 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


• 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.


• 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


• 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.


• 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.


(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.


• 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.


• 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).


• “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.

chapter 9 wakefulness and sleep. rhythms of waking and sleep animals generate endogenous 24 hour...

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