Physiology of sleep and

dreaming
The sleep cycle
Dreaming
Why do we sleep?

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
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.

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
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.
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?
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?
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.
Two interesting variations on
sleep
Cetaceans: No REM
Indus dolphin
Bottlenose dolphin and porpoise
Flocking birds
Gliding birds: swifts and sooty terns
Circadian rhythms
Circadian = diurnal + nocturnal
Zeitgebers and the SCN: Biological clock
Altering light/dark cycles produces phase shift
and entrainment
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
Optic nerve
Optic tract
Lateral geniculate nucleus
Optic radiation
Optic chiasm
Primary visual cortex
Pathways to SCN
CN I
CN III
CN V
CN VII
CN IX
CN XI
CN II
CN IV
CN VI
CN VIII
CN X
CN XII
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.
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.
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.
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
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
More sleep disorders: Sleeping
phases
REM sleep behavior disorder
Slow-wave sleep problems
Nocturnal enuresis
Somnambulism
Pavor nocturnus (Night terrors)
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
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
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.
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
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.
EEG patterns
b
1 a
2 k
3 d
1 sec
EEG patterns...
4 d
1 sec