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.

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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?

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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.

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Two interesting variations on sleep

• Cetaceans No REM
• Indus dolphin
• Bottlenose dolphin and porpoise
• Flocking birds
• Gliding birds swifts and sooty terns

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Circadian rhythms

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

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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

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Optic nerve
Pathways to SCN
Optic chiasm
Optic tract
Lateral geniculate nucleus
Optic radiation
Primary visual cortex
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CN I
CN II
CN IV
CN III
CN V
CN VI
CN VII
CN VIII
CN IX
CN X
CN XI
CN XII
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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.

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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.

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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

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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

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More sleep disorders Sleeping phases

• REM sleep behavior disorder
• Slow-wave sleep problems
• Nocturnal enuresis
• Somnambulism
• Pavor nocturnus (Night terrors)

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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

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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.

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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

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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.

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EEG patterns
b
1 a
2 k
3 d
1 sec
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EEG patterns...
4 d
1 sec