Circadian Rhythms and Sleep in Humans Ppt

5/26/2018 Circadian Rhythms and Sleep in Humans Ppt

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Chapter 9

Wakefulness and Sleep


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Rhythms of Waking and Sleep

Animals generate endogenous 24 hour cycles

of wakefulness and sleep.

Some animals generate endogenouscircannual rhythms,internal mechanisms that

operate on an annual or yearly cycle.

Example: Birds migratory patterns, animals

storing food for the winter.


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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.


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Fig. 9-2, p. 267


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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.


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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.


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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.


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Mechanisms of the circadian rhythms include

the following:

The Suprachiasmatic nucleus. Genes that produce certain proteins.

Melatonin levels.


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The suprachiasmatic nucleus (SCN) is part of

the hypothalamus and the main control center

of the circadian rhythms of sleep andtemperature.

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.


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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.


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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 thatregulate sleep and waking.

Mutations in the Per gene result in odd

circadian rhythms.


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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.


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Melatonin secretion usually begins 2 to 3

hours before bedtime.

Melatonin feeds back to reset the biologicalclock 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.


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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 zeitgeberis a term used to describe any

stimulus that resets the circadian rhythms.

Exercise, noise, meals, and temperature are

others zeitgebers.


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Jet lagrefers to the disruption of the circadianrhythms due to crossing time zones.

Stems from a mismatch of the internalcircadian 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.


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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.


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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.


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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.


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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.


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Mechanisms

Stage 2 sleep is characterized by the

presence of:

Sleep spindles- 12- to 14-Hz waves duringa burst that lasts at least half a second.

K-complexes- a sharp high-amplitude

negative wave followed by a smaller,

slower positive wave.


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Mechanisms

Stage 3 and stage 4 together constitute slow

wave sleep (SWS)and is characterized by:

EEG recording of slow, large amplitudewave.

Slowing of heart rate, breathing rate, and

brain activity.

Highly synchronized neuronal activity.


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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 andfast.

Postural muscles of the body are more

relaxed than other stages.


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Mechanisms

Stages other than REM are referred to as

non-REM sleep (NREM).

When one falls asleep, they progress throughstages 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.


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Mechanisms

Stage 3 and 4 sleep predominate early in the

night.

The length of stages 3 and 4 decrease asthe 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.


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Fig. 9-10, p. 277


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Mechanisms

Various brain mechanisms are associated

with wakefulness and arousal.

The reticular formationis a part of themidbrain that extends from the medulla to the

forebrain and is responsible for arousal.


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Table 9-1, p. 280


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Mechanisms

The pontomesencephalonis a part of the

midbrain that contributes to cortical arousal.

Axons extend to the thalamus and basalforebrain 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.


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Mechanisms

The locus coeruleus is small structure in the

pons whose axons release norepinephrine to

arouse various areas of the cortex andincrease wakefulness.

Usually dormant while asleep.


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Fig. 9-11, p. 279


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Mechanisms

The basal forebrainis an area anterior anddorsal to the hypothalamus containing cellsthat extend throughout the thalamus and

cerebral cortex. Cells of the basal forebrain release the

inhibitory neurotransmitter GABA.

Inhibition provided by GABA is essential forsleep.

Other axons from the basal forebrain releaseacetylcholine which is excitatory and

increases arousal.


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Fig. 9-12, p. 280


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Mechanisms

The hypothalamus contains neurons that

release histamine to produce widespread

excitatory effects throughout the brain.Anti-histamines produce sleepiness.


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Mechanisms

Orexinis a peptide neurotransmitter released

in a pathway from the lateral nucleus of the

hypothalamus highly responsible for theability to stay awake.

Stimulates acetylcholine-releasing cells in

the forebrain and brain stem to increase

wakefulness and arousal.


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Mechanisms

Decreased arousal required for sleep is

accomplished via the following ways:

1. Decreasing the temperature of the brainand the body.

2. Decreasing stimulation by finding a quiet

environment.

3. Accumulation of adenosinein the brain to

inhibit the basal forebrain cells

responsible for arousal.

Caffeineblocks adenosine receptors.


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Mechanisms

(contd):

4. Accumulation of prostaglandins that

accumulate in the body throughout the dayto induce sleep.

Prostaglandins stimulate clusters of

neurons that inhibit the hypothalamic

cells responsible for increased arousal.


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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.


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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.


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Fig. 9-13, p. 281


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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.


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Mechanisms

Insomniais a sleep disorder associated withinability to fall asleep or stay asleep.

Results in inadequate sleep.

Caused by a number of factors includingnoise, 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 inthe circadian rhythms can also result in

insomnia.


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Fig. 9-15, p. 282


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Mechanisms

Sleep apneais a sleep disorder characterizedby the inability to breathe while sleeping for aprolonged period of time.

Consequences include sleepiness during theday, impaired attention, depression, andsometimes heart problems.

Cognitive impairment can result from loss ofneurons due to insufficient oxygen levels.

Causes include, genetics, hormones, old age,and deterioration of the brain mechanismsthat control breathing and obesity.


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Mechanisms

Narcolepsyis a sleep disorder characterizedby frequent periods of sleepiness.

Four main symptoms include:

Gradual or sudden attack of sleepiness.

Occasional cataplexy - muscle weaknesstriggered by strong emotions.

Sleep paralysis- inability to move whileasleep or waking up.

Hypnagogic hallucinations- dreamlikeexperiences the person has difficulty

distinguishing from reality.


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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.


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Mechanisms

Periodic limb movement disorderis 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.


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Mechanisms

REM behavior disorderis 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).


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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.


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Why Sleep? Why REM? Why Dreams?

Functions of sleep include:

Energy conservation.

Restoration of the brain and body. Memory consolidation.


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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.


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Animals also increase their sleep time duringfood shortages.

sleep is analogous to the hibernation ofanimals.

Animals sleep habits and are influenced byparticular aspects of their life including:

how many hours they spend each daydevoted to looking for food.

Safety from predators while they sleep

Examples: Sleep patterns of dolphins,

migratory birds, and swifts.


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Fig. 9-17, p. 287


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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.


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People vary in their need for sleep.

Most sleep about 8 hours.

Prolonged sleep deprivation in laboratoryanimals results in:

Increased metabolic rate, appetite and

body temperature.

Immune system failure and decrease in

brain activity.


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Sleep also plays an important role inenhancing learning and strengtheningmemory.

Performance on a newly learned task isoften better the next day if adequate sleepis achieved during the night.

Increased brain activity occurs in the area ofthe brain activated by a newly learned taskwhile one is asleep.

Activity also correlates with improvement inactivity seen the following day.


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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 inREM.

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.


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Fig. 9-18, p. 289


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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.


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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.


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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.


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The activation-synthesis hypothesissuggests

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 cannotcompete with the self-generated

stimulation and hallucinations result.


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Input from the pons activates the amygdala

giving the dream an emotional content.

Because much of the prefrontal cortex isinactive during PGO waves, memory of

dreams is weak.

Also explains sudden scene changes that

occur in dreams.


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The clinico-anatomical hypothesisplaces lessemphasis on the pons, PGO waves, or evenREM sleep.

Suggests that dreams are similar tothinking, just under unusual circumstances.

Similar to the activation synthesis hypothesisin that dreams begin with arousing stimuli thatare generated within the brain.

Stimulation is combined with recentmemories and any information the brain isreceiving from the senses.


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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 suppressedwhich impairs working memory during

dreaming.


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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.


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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 nocriticism from the prefrontal cortex creates the

hallucinatory perceptions.

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Circadian Rhythms and Sleep in Humans Ppt