Physiology of sleep and dreaming - PowerPoint PPT Presentation

1 / 26
About This Presentation
Title:

Physiology of sleep and dreaming

Description:

Fatal familial insomnia is caused by a dual mutation involving a prion gene PrP. ... Fatal familial insomnia: thalamus damage. Reduction of sleep spindles and ... – PowerPoint PPT presentation

Number of Views:669
Avg rating:3.0/5.0
Slides: 27
Provided by: pauly9
Category:

less

Transcript and Presenter's Notes

Title: Physiology of sleep and dreaming


1
Physiology of sleep and dreaming
  • The sleep cycle
  • Dreaming
  • Why do we sleep?

2
The sleep cycle
  • Electronic recording EEG, EOG, EMG
  • EEG patterns divide sleep into four stages
  • 1 a waves, 8 - 12 Hz, low amplitude, moderate
    frequency, similar to drowsy wakefulness
  • 2 slower frequency, higher amplitude, plus
  • K complexes
  • Sleep spindles
  • 3 d waves appear, 1-2 Hz, large amplitude
  • 4 Dominated by d waves

3
REM sleep phenomena
  • Stage 1 EEG Paradoxical sleep
  • EOG (and corneal bulge) show frequent eye
    movements, as if scanning a visual field.
  • EMG shows loss of muscle tonus due to downward
    inhibition of a motor neurons, although muscles
    moving hands and feet may twitch.
  • Many brain structures function as if awake.

4
More REM phenomena
  • SNS is partially activated Increases blood
    pressure, respiration, and heart rate.
  • Genital response
  • Narrative dreaming
  • CBF is high to visual cortex, low to inferior
    frontal cortex (Madsen, 1991)
  • Eye movements match dream events
  • One EEG waveform is unique to REM and wakeful
    scanning

5
Dream research
  • External stimuli may be incorporated into a
    dream.
  • Dream events happen in real time.
  • Everyone dreams recall depends on when in the
    sleep cycle you awaken.
  • Genital response is independent of dream content.
  • Sleep-walking and talking are non-REM.

6
Interpretation of dreams
  • Manifest content is symbolic of latent desires
    (Freud)
  • Activation-synthesis theory cf. incorporation of
    external events into dreams.
  • Lucid dreams Have you had one?

7
Why do we sleep?
  • Restoration, recuperation or repair
  • Waking life disrupts homeostasis
  • Sleep may conserve some energy
  • Protection with the circadian cycle
  • Circadian synthesis
  • Consolidation of learning?

8
Who sleeps?
  • Mammals and birds
  • Opossums, sloths, bats 19-20 hours daily
  • Cats, dogs, rodents 12-15 hours daily
  • Ruminant herbivores 2-3 hours daily
  • Reptiles, amphibians, fish, and insects have
    cycles of inactivity
  • Note that sleep time does not correlate with
    waking activity levels, but does relate to waking
    vulnerability.

9
Two interesting variations on sleep
  • Cetaceans No REM
  • Indus dolphin
  • Bottlenose dolphin and porpoise
  • Flocking birds
  • Gliding birds swifts and sooty terns

10
Circadian rhythms
  • Circadian diurnal nocturnal
  • Zeitgebers and the SCN Biological clock
  • Altering light/dark cycles produces phase shift
    and entrainment

11
Evidence for the SCN as biological clock
  • Free-running rhythms and the 24 hour period
  • SCN lesions disrupt circadian rhythms
  • SCN tissue maintained in vitro retains cyclicity
  • Transplanted SCNs set rhythms of donor animal
  • Recall the pathway in the visual system from
    retina to SCN These retinal ganglion cells
    contain a photopigment, melanopsin, and are light
    sensitive

12
Optic nerve
Pathways to SCN
Optic chiasm
Optic tract
Lateral geniculate nucleus
Optic radiation
Primary visual cortex
13
CN I
CN II
CN IV
CN III
CN V
CN VI
CN VII
CN VIII
CN IX
CN X
CN XI
CN XII
14
The Per-Cry-Tau complex
  • In mammals, two SCN proteins (Clock and Cycle)
    form a dimer.
  • The Clock/Cycle dimer acts on DNA to enhance
    transcription of Period (Per) and Cryptochrome
    (Cry).
  • Per and Cry bind in a complex with Tau
  • The Per-Cry-Tau complex inhibits the Clock/Cycle
    dimer, slowing Per-Cry production
  • Per-Cry breakdown over 24 hours allows a new
    cycle to start.
  • Melanopsin-containing ganglion cells release
    glutamate in the SCN, increasing per
    transcription and entraining the SCN.

15
Genetic variations
  • Variations in the Clock gene may distinguish
    morning people from evening people
  • Fatal familial insomnia is caused by a dual
    mutation involving a prion gene PrP.
  • Found in 40 families worldwide
  • Mean onset age 50
  • Death ensues 7 to 36 months later.

16
Effects of sleep deprivation
  • Sleep deprivation within a circadian cycle is
    followed by less sleep, not more
  • Internal desynchronization free-running body
    temperature cycle and sleep-wake cycle may
    desynchronize.

17
Resynchronization
  • Jet lag and shift work
  • Phase shift Delay is better than advance
  • Morning melatonin phase-delays
  • Afternoon melatonin phase-advances
  • Evening melatonin is ineffective
  • Bright light exposure has the opposite effects
  • Strengthen zeitgebers like light and activity
    early in the new waking period

18
Sleep disorders
  • Waking phase disorders
  • Insomnia
  • Drug-dependency insomnia
  • Sleep apnea PAP or surgery
  • Fatal familial insomnia thalamus damage
  • Reduction of sleep spindles and K-complexes
  • SIDS
  • Narcolepsy
  • Cataplexy
  • Decreased hypocretin neurons
  • Sleep paralysis
  • Hypnagogic hallucinations

19
More sleep disorders Sleeping phases
  • REM sleep behavior disorder
  • Slow-wave sleep problems
  • Nocturnal enuresis
  • Somnambulism
  • Pavor nocturnus (Night terrors)

20
Overall sleep deprivation
  • Under total, voluntary sleep deprivation,
    sleepiness is cyclical
  • Greatest sleepiness from 3-6 a.m.
  • Waking sleepiness is countered by activity
  • Sleepiness increases only up to four days
  • Active, complex tasks are not impaired
  • Easy, boring tasks are impaired
  • Microsleep emerges

21
Compensation for sleep deprivation
  • Subsequent slow-wave, non-REM sleep is increased
  • Stage 3 and 4 sleep is almost completely restored
  • Involuntary sleep deprivation is stressful
  • Executive rats on a carousel apparatus died
  • Post-mortem exams showed few of the usual stress
    symptoms

22
REM deprivation
  • REM pressure
  • REM rebound
  • REM escape
  • Three theoretical effects
  • Mental disorder
  • Amotivational syndrome
  • Memory processing deficits
  • But tricyclic antidepressants block REM with none
    of these side effects.

23
Neural control of sleep
  • Is sleep a passive process?
  • The cerveau isole of Bremer (1936) SWS only
  • The encephale isole and the RAS normal sleep
  • Partial transections leaving the RAS intact
  • Ventrolateral Preoptic Area (VPA) triggers
    sleepiness and slow-wave sleep
  • Warming the basal forebrain induces slow-wave
    sleep GABA on tuberomammillary nucl.
  • VPA receives input from thermoreceptors

24
More neural control
  • PGO waves in the EEG from implanted electrodes
  • Executive in the dorsolateral pons, called the
    peribrachial area.
  • Kainic acid lesions of peribrachial area reduce
    REM sleep
  • Carbachol, an ACh agonist, in ventral pons
    (medial pontine reticular formation) triggers REM
    phenomena.

25
EEG patterns
b
1 a
2 k
3 d
1 sec
26
EEG patterns...
4 d
1 sec
Write a Comment
User Comments (0)
About PowerShow.com