AROUSAL AND SLEEP

LEENA.S.T DEPARTMENT OF PSYCHOLOGY

AROUSAL
Arousal is a physiological and psychological

state of being awake It involves the activation of : 1.reticular activation system 2.autonomic nervous system 3.endocrine system

Actvation of these 3 systems leads to

1.Increase heart rate 2.Blood pressure

3.Sensory alertness
4.Mobility 5.Readiness to respond

Arousal system
1.Originates from brain stem with connectons extending throughout the cortex 2.Connections are based on neuro transmitters A.Acetyl choline B.Norepinephrine C.Dopamine D.serotonin

Arouasl is imporatant in regualting.

1.consciousness 2.Attention

3.Information processing
4.Mobility 5.Flight or fight response

6.Sexual activity

Yerkes-Dodson law
Shows the relationship between arousal and

performance

SLEEP
Sleep is as critical to survival as eating

&drinking It has an on signal & offsinal Sleep is not a unitary process Circardian rhythm Sleep deprivation results in hallucinations Signals thought to be initiated internally Manipulation of external cues has little effect on the sleep awake cycle

Blood factor & sleep

Sleep served to

restore neural energy depleted by fatigue

Toxine theory & sleep

During waking hours fatigue toxins

accumulate and when these toxins exceed a given optimum level they trigger sleep

It is said that fatigue signal is in blood

Neural factor and sleep: ( study by Bremer in 1935)

Surgically removed sensory inputs to the

brain and observed resulting EEGs recorded from cortex

Encephale isole-cut between brain stem

and spinal cord 1.all sensory input was eliminated from below neck 2.EEG activity still revealed normal sleep wake patterns

 Cerveu isole
1.Upper part of the brain stem and mid brain level 2.Optic and olfactory nerves left intact 3.Cut indeed abolish waking activity 4.Thes e indicate that sleep wake cycle depends upon neural input from sensory systems

 Cut at midbrain level reduces the amount of

sensory stimulation reaching the cortex It detaches connection from other parts of brain stem

Wake center
Donald Lindsleymidbrain reticular lesion-

abolished wakefulness
Moruzzi& magoun

electrical stimulation of midbrain reticular formation wakefulness

Wake center
1.sensory input is not necessary to maintain

sleep wake cycle What is signal? Wake center 1. midbrain reticular formation 2.center turns wakefulness on 3.when damaged it turns wakefulness off

The neural mechanism of sleep

Michael Jouvet 1.passive theory-sleep is a passive

phenomenon ,like slowing a car Sleep is caused by activity in the wake center dying out because of fatigue Active theory-sleep is caused by sleep area actively inhibiting wake area

Sleep circuit
Walter Hess has illuminated a complex sleep

circuit stretching from the lower parts of the brainstem to the thalamus and cortex

Sleep circuit
In order to be a sleep circuit it should ful fill It must produce sleep when stimulated

Must produce wakefulness when removed

Hess & others found that low frequency

electrical stimulation in the medial thalamussleep Subsequent studies-sleep control not confined to the medial thalamus only

Other areas involved in sleep

1.non specific projection nuclei of thalamus 2.preoptic area in the hypo thalamus 3.several areas in the lower brain A. pontine reticular formation Raphe nucleus

Stimulation in all these areas -sleep Lesion in preoptic area - insomnia

Sleeping and EEG pattern

Sleep is not an unitary process

It has different depths and stages

Analysis is possible by distinct EEG activity

awaken brain -EEG

pattern

awaken brain 1.show very fast activity 20-25 cps (beta waves) 2.awaken neurons are active in a random fashion 3.The fluctuations in voltage are so out of phase that they tend to cancel one another out and produce desynchronized low amplitude waves

Brain falls asleep

Pattern of activity undergoes a pronounced

transformation Waves become much larger and much slower Moves from 8 to 10 per second (alpha) As person relaxes 2 or 3 cps (delta) Then the person falls into deep sleep

 Slow wave sleep -80% of sleeping hours 20%-paradoxical sleep

Paradoxical sleep-brain shows waking state

even though body remains asleep

 During paradoxical sleep there is fast

,desynchronized,low amplitude activity in cortex and most of subcortex Exception is hypocampus which shows a slow regular rhythm known as theta waves The body is even more relaxed during paradoxical sleep than during slow wave sleep,as evidenced by the reduction in muscle tone

 Its very harder to wake a person from

paradoxical sleep than from slow wave sleep

Dreaming & EEG.

During paradoxical sleep that dreaming

occurs(Nathaniel kleitman&collegues) Dreaming is marked by fast low amplitude EEG activity in the cortex Eye balls move during dreaming Rapid eye movement sleep_ the stage of sleep where eyeball move as if a person were following a moving object with his eyes

 Most people awakened during REM sleep

report dream This does not mean that dreaming only occurs at paradoxical sleep Dreaming also occur during slow wave sleep

Musle relaxation
It may serve as an important safety device

Apparently the limb body during paradoxical

sleep reflects an active inhibitory mechanism in the brain that may protect determines from acting out their dreams

Behavioral nightmares
Jouvet damage to locus of coeruleus

produce behavioral night mares The eyes of the cat in the middest of this nightmare are close d and its behavior has no relationship to external events The cat becomes extremely active It hisses and claws as if acting out a dream

Neural control of paradoxical sleep and slow wave sleep-Jouvet

Jouvet concentrated on

the neural control of sleep

He given special attention

to brain stem

His subjects were cats as

cats shows both types of sleep

Paradoxical sleep-Jouvet
During paradoxical sleep cats show unique

spike ie;patterns reffered to as PGO spikes According to Jouvet Paradoxical sleep is controlled by pontine
reticular formation (nucleus reticularis pontis caudalis) Lesion abolish REM sleep Stimulation induce REM sleep

Slow wave sleep

Slow wave sleep is controlled by the area in

brain stem raphe nucleus Lesion abolish slow wave sleep Stimulation - induce slow wave sleep Slow wave sleep depends on both raphe nucleus & its interaction with the cortex Paradoxical sleep primarily depend upon the pontine reticular formation

Raphe neucleus and reticualr formation

Cortex and slow wave sleep

Animal CNS is incomplete at birth ,show only

paradoxical activity during sleep Paradoxical activity in the brain stem As cortex develops slow wave activity appears during sleep Eg:pigs neural development including cortex is virtually complete at birth Pigs show both paradoxical sleep and slow wave sleep at birth

Chemical codes for sleep

Raphe nucleus-serotonin(neuro transmitter) Serotonin control slow wave activity

Elevating serotonin level will result in increased sleep time at day time for the normal animals Elevated serotonin level but lesion raphe nucleus serotonin compensate for lesion and restore normal slow wave activity.

Pontine reticualr formation and chemical codes

Pontine reticular formaton (areas related with

paradoxical sleep)- contain norepinephrine Elevating norepinephrine increased day time paradoxical sleep Elevating norepinephrine by lesioning pontine reticuar pormation-compensate for pontiner eticular formation &restores paradoxical sleep

Interaction between slow wave sleep &paradoxical sleep

Both sleeps are under the control of different

neural areas and chemical processes Paradoxical sleep depends n some minimal amount of slow wave sleep Eg;eliminating slow wave sleep by lesioning Raphe nucleus abolish paradoxical sleep Lesioning of pontine reticular formation does not have any effect upon slow wave sleep

Conclusion -Jouvet
He arrived at a hypothesis to explain the

interrelationship between the 2 types of sleep Postulated that during slow wave sleep serotonin metabolized Its metabolized by the Raphe nucleus And its break down products prime the pontine reticular formation It release norepinephrine and produce paradoxical sleep

Complicating pictures
It is not complete explanation for sleep Acetyl choline too has pronounced effects on

sleep &wake When acetyl choline injected into preoptic area, pontine reticular formation it affected sleep and wake Serotonin source of slow wave sleep Depletion serotonin level disrupts sleep But animals recovers noramal pattern of sleep though serotonin level remain below normal

 Neural mechanism that coordinate the cycle

between sleep and wake remain as open question

DREAM
Human have a strong need to dream (studies) The function of dream is still not clear Roffwarg has theorized that paradoxical sleep has an important adaptive function Stimulates neural growth during formative periods

He explained why infants show more paradoxical sleep than adults

REM rebound-sleep experiment

An individual deprived of dreaming becomes

irritable and when finally allowed to sleep shows a significant increase in paradoxical sleep as if making up for lost dreams The compensatory dreaming following deprivation is known as REM rebound Subject behaves like a deprived organism Subjects becomes irritable &confused

They have difficulty in concentration They undergo memory lapses And develop strong appetite for food Then finally allowed to sleep They dream an abnormal amount as much as 60%more than normal Then finally returns to normal NB: (subject was awakened immediately upon slipping into paradoxical sleep)

Developmental implications of dreaming

Children spent more time in paradoxical

sleep than adults

Children-50% Adults-20%

Experts studied developmental implications of dreaming

Howard Roffwarg and collegues

David kretch and collegues

Howard and collegues .

Dreaming is related with mental growth and

development Evidence shows that stimulation from external environment influences growth during maturation

David kretch & collegues

Rats reared in enriched sensory environment

show larger brains than those reared in an impoverished sensory environment. Dreaming is a form of self stimulation. Dreaming promote the growth of the brain during the early formative years.

Dreaming and mental illness

The major study is of Dement Study was on cats

Dement injected parachlorophenylalanine & depleted serotonin(which directly initiate slow wave sleep and then paradoxical sleep) Depletion resulted in general decrease in sleep
Paradoxical sleep spilled over into

wakefullness

 First PGO spikes appeared in awaken state 2nd dream like state appeared in awaken state Cats perked their ears &struck out at objects

that werennt there They were like hallucinating These cats(Dements cats)didnt shown rebound effect Human schizophrenics also dont have rebound effect

 It can be abolished by administering

chlorpromazine Chlorpromazine is the effective medicine for schizophrenia today Even when we cant say that shizophrenia is the result of depleted serotonin levels in brain Hallucinating behavior spills over to waking hours

 Role of serotonin in schizophrenia remain an

open & controversial question

Sleep disorders- insomnia

20% of US population experience sleep

disorders Insomnia-inability to sleep

Short tern insomnia-stress,drinking ,too

much coffee etc

prevention
Improving sleep habbits Avoiding stimulants

Avoid taking sleepin pills

More serious insomnia is associated with

psychiatric disorders(depression)

Sleep apnea
Interrupted breathing during sleep A person suffering from sleep apnea may

awaken 100s of times during the night Results in no slow wave sleep &less time in REM sleep These patients are chronically tired in the day time and often suffer from depression

 Sometimes sleep apnea leads to sudden

death Airway collapses during breathing &then blocking air flow

Restless legs syndrome

Its a common problem

Familial disorder
Unpleasant crawling Prickling

Tingling sensations in the legs and feet

Urge to move about for relief

Narcolepsy
Characterizd by frequent REM sleep attacks

during day time They enter REM sleep from wakefulness without going through non REM sleep.