SLEEP & CIRCADIAN RHYTHMS

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Presentation transcript:

SLEEP & CIRCADIAN RHYTHMS Images in these slides were obtained from the following sources: Carlson, Physiology of Behavior, 9th edition (2007) Allyn and Bacon Rosenzweig, Leiman and Breedlove, Biological Psychology (2001) Sinaur Associates, Inc

SLEEP PHYSIOLOGY PHYSIOLOGICAL MEASURES Electroencephalogram (EEG) brain waves from scalp surface Electrooculogram (EOG) eye movements Electromyogram (EMG) muscle tone

SLEEP PHYSIOLOGY EEG Waves (wakefulness) beta waves alpha waves Irregular low amp., high freq. waves (13-30 Hz) indicative of alert and vigilant activity alpha waves regular medium freq. waves (8-12 Hz) resting quietly, but awake

SLEEP PHYSIOLOGY SLEEP STAGES Stage 1: alpha and theta waves (initial) Stage 2: K complexes, sleep spindles Stage 3: 20-50% delta (SWS) Stage 4: > 50% delta (SWS) REM (emergent stage 1)

SLEEP PHYSIOLOGY REM SLEEP increased cerebral activity, erratic EEG (beta and theta waves) rapid eye movements loss of core muscle tone (paralysis) autonomic arousal (elevated hr, bp, and respiration) narrative dreams with much visual imagery initially referred to as “PARADOXICAL SLEEP”

SWS VS. REM SLEEP

SLEEP CYCLES

SLEEP PATTERNS Percent of SWS vs. REM changes with age Young Adult sleep patterns consist of: 7-8 hours of 90-110 min. repeating cycles 45-50% of total sleep is stage 2 20% of total sleep is REM sleep More SWS early in night Progressive lengthening of REM periods

LIFE SPAN CHANGES IN SLEEP Daily sleep rhythms begin ~ 16 weeks. Greater % REM in infants and children. REM component decreases with age. Total sleep time decreases with age. Elderly frequently experience insomnia and decreased SWS.

LIFE SPAN CHANGES IN SLEEP

SLEEP DISORDERS INSOMNIA affects ~25% of population occasionally, ~9% regularly No single definition Insomnia is symptom, not a disease multiple causes, often iatrogenic tolerance to sedative-hypnotic drugs frequent symptom of depression Other causes: sleep apnea, nocturnal myoclonus, restless legs (PLMD)

SLEEP DISORDERS Sleep-onset insomnia Sleep maintenance insomnia difficulties falling asleep Sleep maintenance insomnia frequent awakenings, may be associated with SLEEP APNEA (difficulty breathing while asleep)

SLEEP DISORDERS NARCOLEPSY Characteristic Symptoms: Sleep Attack (5-30 minutes) Cataplexy frequently brought on by intense emotions Immediate REM at sleep onset Sleep Paralysis Hypnogogic Hallucinations

SLEEP DISORDERS NARCOLEPSY Heritability and Hypocretin (Orexin) Genetic models in dogs increased ACh receptors in pons amygdala and forebrain degeneration canarc gene (Hypocretin 2 receptors) Hypocretin gene knockout mouse model CSF analysis in human narcoleptic patients show diminished hypocretin levels.

SLEEP DISORDERS REM SLEEP BEHAVIOR DISORDER Characterized by failure to exhibit muscle paralysis during REM sleep Appears to be neurodegenerative disorder with some possible genetic component Often associated with other neurodegenerative disorders, such as Parkinson’s disease Usually treated with clonazepam, a benzodiazepine

SLEEP DISORDERS COMMON CHILDHOOD SLEEP DISORDERS ASSOSCIATED WITH SLOW WAVE SLEEP Pavor Nocturnus (night terrors) Somnambulism (sleep walking) Nocturnal Enuresis (bed wetting)

SLEEP FUNCTIONS (Why do we sleep?) Restorative Functions growth and repair Adaptive Functions predator avoidance energy conservation Cognitive Functions learning, unlearning, reorganization

COMPARATIVE STUDIES OF SLEEP

SLEEP IN MARINE MAMMALS

SLEEP DEPRIVATION Early reports of bizarre or psychotic behavior Wide individual variability (personality and age factors) Most common effects of sleep deprivation: increased irritability decreased concentration Confusion/disorientation

SLEEP DEPRIVATION IN HUMANS Performance on brief tasks is unimpaired. Performance on tasks that involve high motivation are generally not impaired. Sleep Recovery (Randy Gardner story) 11 days (264 hours) sleep deprivation 1st night, ~ 15 hours; stage 4 increased at expense of stage 2 2nd night, ~10 hours; greatest REM recovery Percentages of sleep recovery not equivalent across all stages: 7% of stages 1 and 2, 68% SWS, 53% REM sleep “made up”

SLEEP DEPRIVATION IN NONHUMANS It is difficult to tease apart effects of sleep deprivation versus stressful effects of the procedure. Rechtschaffen and Bergmann, 1995 Carousel apparatus with yoked controls Experimental animals died within days, while controls remained relatively healthy.

EFFECTS OF ACTIVITIES ON SLEEP Effects of Exercise on Sleep Does the brain recover from day time physical exertion? Little compelling evidence: People who spend much of their time resting in bed do not sleep less Effects of Mental Activity on Sleep Does the brain recover from day time mental exertion? Some studies have shown that extensive mental activities are followed by normal sleep duration, but increased SWS.

FUNCTIONS OF REM SLEEP Theories that REM sleep is required for normal Mental health Motivation Cognitive processing Interesting links between REM sleep and depression REM deprivation has antidepressant effects Most antidepressant drugs also reduce REM sleep. There’s considerable research on links between REM sleep and learning/memory.

REM SLEEP DEPRIVATION Following REM deprivation, there is a compensatory increase in REM sleep, which seems to suggest REM sleep is a necessary brain function. Some evidence that REM deprivation can produce cognitive/memory deficits. Some evidence that REM sleep increases following new learning.

NEURAL MECHANISMS OF SLEEP Basal Forebrain Brain Stem Reticular Formation Raphe nucleus (midbrain) Locus Coeruleus (pons) Lateral hypothalamus

NEURAL MECHANISMS OF SLEEP Sleep is an active state mediated by at least three neural systems Forebrain: generates SWS Reticular Formation: Wakes Forebrain Pons: Triggers REM sleep

NEURAL MECHANISMS OF SLEEP Bremer (1935) Encephale isole Cerveau isole Moruzzi and Magoun (1949) Reticular formation Jouvet (1967) Raphe system

NEURAL MECHANISMS OF SLEEP BASAL FOREBRAIN ventral frontal lobe, anterior hypothalamus lesions abolish SWS electrical or heat stimulation can induce SWS activity These neurons are active at sleep onset Inhibited by NE stimulation

NEURAL MECHANISMS OF SLEEP RETICULAR FORMATION central core of brain stem diffuse group of cells extending from medulla to thalamus electrical stimulation produces arousal, awakens a sleeping animal lesions produce persistent sleep

NEURAL MECHANISMS OF SLEEP RAPHE NUCLEI A system of serotonergic neurons along midline of brain stem. Lesions to Raphe nuclei produce insomnia. PCPA inhibits 5-HT synthesis and reduces sleep, whereas 5-HT agonists promote sleep

NEURAL MECHANISMS OF SLEEP PONS crucial for REM sleep components lesions ventral to Locus Coeruleus abolish REM sleep electrical or pharmacological stimulation (ACh agonists) can induce or prolong REM sleep small lesions ventral to LC selectively abolish REM muscle atonia

NEUROTRANSMITTERS AND SLEEP

CIRCADIAN RHYTHMS DEFINITION EXAMPLES 24 hr. endogenous cycles sleep/wake cycle body temperature hormone secretion drug sensitivity

LABORATORY STUDIES OF CIRCADIAN RHYTHMS

CIRCADIAN RHYTHMS TERMINOLOGY Free Running Period Entrainment Zeitgeber Phase Shifts phase advances: acceleration of circadian rhythm phase delays: deceleration of circadian rhythm

CIRCADIAN RHYTHMS Circadian Timing Mechanisms Internal desynchronization of S-W cycle and body temp. cycle suggest separate timing mechanisms. Common Examples of Phase Shifts Jet Lag results from phase shifts in circadian rhythms as a result of traveling across time zones. Shift workers often forced to adjust S-W cycle. Such disruptions may affect health and productivity.

NEURAL MECHANISMS OF CIRCADIAN RHYTHMS

SUPRACHIASMATIC NUCLEUS Experimental Research on SCN involvement in circadian rhythms Large lesions of hypothalamus disrupt circadian cycles of activity in rats. (Richter, 1967) Lesions specific to SCN disrupt periodicity of sleep/wake cycle SCN displays circadian cycles of electrical, metabolic, and biochemical activity. Fetal tissue transplants in hamsters Fetal tissue from 20 hour donor implanted in 25 hour recipient after SCN lesion. Recipient becomes entrained to 20 hour cycle

SUPRACHIASMATIC NUCLEUS