PY460: PY460: Physiological Physiological PsychologyPsychology

Chapter 9: Rhythms of Wakefulness & SleepRhythms of Waking & SleepingStages of Sleep and Brain MechanismsWhy Sleep? Why REM? Why Dreams?

Slide 2: Natural Cycles of Biological Activity

[Clip: The Brain- Sleep & Circadian Rhythms] Curt Richter (1920’s)- biological beings have

naturally occurring biological cycles largely independent of the outside world. Challenge to behaviorism in the mid-1900’s

why?

Endogeneous cycles- of evolutionary value anticipation of upcoming conditions

migration mating storage

“migratory restlessness” in willow warblers occurs despite lack of environmental cues (light)

Slide 3: Specific Endogenous Cycles

Endogenous Circannual Rhythms internal cycles that prepares animal for

seasonal changes storage of fats, hibernation, humans???

Endogenous Circadian Rhythms internal cycles (rhythms) that prepares animal

for changes that last about a day. Most Familiar Rhythm? Sleep & Wakefulness!

Others include: core body temperature, frequencyt of eating & drinking, hormonal secretion, chemical sensitivities (drugs).

Slide 4: Zeitgebers: Keeping Rhythms in Synchrony

All rhythms typically stay in synchrony suggesting a “master biological clock” exists (more on this in a bit).

We know that our free running rhythms are often greater than 24 hrs. (24.25- 24.75 hrs.).

Why don’t we (and other animals) get “off-pace” with the 24 hours daily cycle?

AH…LIGHT the primary Zeitgeber (say like a German)- resets the master clock. other “time keepers”- noises, meals,

temperature variations

Slide 5: Mammoth Cave etc.- Altering the Biological Clock?

What is humans traveled to a planet with a different daily cycle (say 20-30 hrs)? How would we adjust?

Mammoth Cave study (1963). A month in a cave (temperature and light controlled). 28 hr days, (9 hrs sleep). What would happen to their cycle? Findings: Continued maintenance of the 24 hour clock…

subjects could force themselves into the schedule but, bodies maintained original rhythms.

Study 2: 12 volunteers in a cave… clock varied between 24-22 hours.. At 23 hrs most subjects adjusted, only 1 @ 22 hrs.

Bottom Line- significant changes in daily rhythms very difficult to make

Slide 6: Disturbing the Biological Clock

Our free running clock runs longer than 24 hrs, but our days are 24 hrs… daily readjustment keeps us in sync...

What would changes might cause de-synchrony between biological clock & hourly clock?

WEEKENDS (No.1)-- Fewer time constraints… Often follow bioclock---

Go to bed later, sleep in…get up.. Reset clock.. Go to bed later than before.. Get up little later.. Reset clock-- by Monday, bioclock hours behind the hourly clock

SHIFT WORK-- night shifts, or irregular pattern in schedule lead to irregular sleeping patterns, temperature often maintain daily pattern, health & safety issues. Particularly bright light somewhat effective in

competing with day time light

Slide 7: More Disturbances in the Bioclock

JET LAG- rhythm disturbance caused by crossing times zones.. Traveling west (PA to LA) (stay up later, sleep in… gain

hours )(27 hrs… tend to be ok-- more natural to be awake a little later.. Sleep in)

Traveling East (LA to PA) (lose hours).

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Slide 8: Suprachiasmatic Nucleus- the bioclock Suprachiasmatic Nucleus- area in the hypothalamus, just

above the optic chiasm (nerve).Rentinohypothalamic pathway Autorhythmic quality may drive circadian rhythms.

Biological clock stops if damaged or Optic Nerve projecting to SCN is damaged

Extremely sensitive to light (even in blind moles!) SCN reset to light

– Biochemical action unclear.. Protein production?

Slide 9: SCN & Melatonin

Melatonin- hormone important in regulating sleepiness & wakefulness secreted near the end of a waking cycle.. A few hours before

typical bed time. Pineal Gland- secretes melatonin release at the

command of SCN. Taking melatonin supplements (.5 mg) in the afternoon--->

phase-advances circadian rhythm (jet lag?) Taking melatonin in morning phase-delays circadian rhythm

A note of warning-- little extended research in area.

Slide 10: The Brain During Sleep (NREM Sleep only)

EEG- increased wave size= greater synchrony between two close sites on cortex. Provides an objective measure of sleep and wakefulness

Stages of Sleep- characterized by a type of wave Awake/Relaxed- Alpha Waves, Beta Waves Stage 1: freq. irregular, jagged waves (Theta) Stage 2: Sleep Spindles (12-14hz) & K-complexes

K-complexes evoke by sudden stimuli (noise etc) Stage 3 & 4: Slow wave sleep (SWS) (2hz waves)

» big slow waves (delta) indicating high synchrony

» reduced sensory input to cortex… “less noise”

» see wave and stone analogy (p. 254)

Slide 11: Synchrony & EEG

Choose the stage &name the characteristics

•Big slow 1/2 sec waves; highly synchronous action

•Alpha & beta waves (smaller amplitude) regular and choppy respectively

•sleep spindles & k-complexes frequent here

Slide 12: REM Sleep/Paradoxical Sleep

Michel Jouvet, Kleitman & Aserinsky- scientists notice that during certain intervals of sleep high levels of brain activity (almost looked awake) no bodily movement though, in fact most relaxed state of

postural muscles rapid eye movement in humans increased “genital activity” called it “paradoxical” and “REM” sleep, respectively.

REM sleep-- low voltage, irregular waves suggestive of considerable brain activity

Slide 13: Cycling through the stages

Progression through the stages @ night.

Stage 3 to 4 longest early on

progressive lengthening of REM toward the final hours

REM strongly associated with dreaming.. But apparently not the only dream stage

Slide 14: Brain Structures in Wakefulness & Arousal

The Reticular Formation- structures whose length extends from the spinal cord up to the forebrain.. Widely connected to the sensory systems

» may easily respond to slightest sensory impulse

Spontaneous pulsing activity regulating arousal even with little external stimuli

Cutting through the midbrain immediately reduces arousa Pontomesencephalon- Locus Coeruleus- emits arousing bursts to meaningful

events such as reinforcement/arousal and may assist in memory of important events.

Inactive during sleep-->little memory??

Slide 15: “Arousing Brain Structures” continues

Basal Forebrain (anterior and dorsal to hypothalamus)

Damage leads to decreased arousal, impaired learning & attention

most damaged by degradation of Alzheimer’s Acetylcholine- an arousing neurotransmitter in BF

GETTING TO SLEEP- Inhibiting Arousal Systems Adenosine (declines during sleep) - a neuromodulator that

accumulates over the course of the day and blocks ACh. Caffeine- blocks Adenosine--> incr. Arousal (ACh)

interferes the whole day… even a morning cup of “Joe”. Prostaglandins- (decline during sleep)

Slide 16: Brain Functions in REM Sleep: PGO Waves

The first indication of approaching REM sleep are short burst from the Pons, lateral Geniculate, & Occipital Cortex (PGO waves) (see text figure 9.12) LG and OC critical for vision processes-- REM primarily a

visual phenomenon? First part of REM--- LG / OC manipulation Latter-- more thalamus than just LG and the

cerebral cortex… becomes a less visual phenomena.

Pons-- pulses related to sleep paralysis damage to Pons cell to the spinal cord leads to

disinhibtion of behavior during sleep (fig 9.13).

Slide 17: Abnormalities of Sleep/Insomnias

Causes: many caffeine, drugs, stress,

temperatures Onset insomnia Maintenance Insomnia Termination Insomnia

Irregularities in biorhythms phase delayed

» onset an issue

phase advanced» termination an

issue

Slide 18: Other Abnormalities of Sleep

Sleep Apnea- inability to breath during sleep-- cuts sleep times in half in worst cases…. Linked to obesity

SIDS Narcolepsy- intrusion of REM into “wakeful”states

sudden sleepiness during day cataplexy- muslce weakness while awake frequent sleep paralysis even during “twilight” states Hypnogogic hallucinations on early onset.

PLMD- decr sleep paralysis (Pons?) REM Bhvr Disorder-act out dreams (damage to pons & midbrain) Night Terrors-screaming in terror during NREM sleep Talking in Sleep (REM or NREM sleep) Sleepwalking- strong genetic component

» awakening sleep walkers

Slide 19: What is sleep for? Theories on Function

Repair & Restoration Theory- Sleep evolved to assist the body in repairing itself after the exertions of the day.

Going without sleep-- psychological effects (what are they?)

Physiological f/x: increased body temp, metabolic rate, appetite; decreased immune response.

Evolutionary Theory of Sleep- a form of mini-hibernation… we sleep when food is scarce and danger is greater.. Conserves energy when we can’t replenish it easily or safely. Temp decreases, metabolism decreases Carnivores/Herbivores sleep patterns

Slide 20: The Function of REM- What is it good for?

Abundance of REM during early childhood» neuronal connections?? (see fig 9.17, pg276)

REM varies from person to person.. It has been suggested we could go without it (Horne, 1988).

So what if we do go without?? (Dement, 1960) Dement woke subject for a week every time went into REM

stage effects: decreased time to REM sleep.. Up to an average of

26 times of waking per night by 7 day up from 12 on the first effects: increased anxiety, decreased concentration,

personality change, increased appetite/weight gain. Cat research

other hypotheses on roles of REM sleep REM assists in memory formation Increased oxygen delivery to retina’s

Slide 21: A Biological Perspective on Dreaming

Freud- Dreaming symbolic of unconscious wishes (“wish fulfillment”)

Activation-synthesis hypothesis- various external stimuli activate structures in the brain and are synthesized by the brain into a “story”.

Is this sensible to you… how have external stimuli been incorporated into your dreams?

Another version.. The brain is active during REM sleep but starved for stimuli.. In this absence---> borrows aspects from memory to construct a story. Flying sensations (vesitbular pulses) Slow movement dreams (postural muscles frozen)

Clinico-Anatomical Hypothesis Dreams begin with arousing stimuli from the brain’s own

motivations, memories, and arousal Does not compete with visual input or censorship by

prefrontal cortex