PY460: Physiological Psychology

1. PY460: Physiological Psychology • Chapter 9: Rhythms of Wakefulness & Sleep • Rhythms of Waking & Sleeping • Stages of Sleep and Brain Mechanisms • Why Sleep? Why REM? Why Dreams?

2. 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)

3. 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).

4. 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

5. 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

6. 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

7. 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).

8. 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?

9. 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.

10. 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)

11. 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

12. 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

13. 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

14. 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??

15. 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)

16. 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).

17. 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

18. 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

19. 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

20. 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

21. 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