Chapter 9 Wakefulness and Sleep Rhythms of Waking and Sleep • Animals generate endogenous 24 hour cycles of wakefulness and sleep. • Some animals generate endogenous circannual rhythms, internal mechanisms that operate on an annual or yearly cycle. – Example: Birds migratory patterns, animals storing food for the winter. Rhythms of Waking and Sleep • All animals produce endogenous circadian rhythms, internal mechanisms that operate on an approximately 24 hour cycle. – Regulates the sleep/ wake cycle. – Also regulates the frequency of eating and drinking, body temperature, secretion of hormones, volume of urination, and sensitivity to drugs. Fig. 9-2, p. 267 Rhythms of Waking and Sleep Circadian rhythms: • Remains consistent despite lack of environmental cues indicating the time of day • Can differ between people and lead to different patterns of wakefulness and alertness. • Change as a function of age. – Example: sleep patterns from childhood to late adulthood. Rhythms of Waking and Sleep • Experiments designed to determine the length of the circadian rhythm place subjects in environments with no cues to time of day. • Results depend upon the amount of light to which subjects are artificially exposed. – Rhythms run faster in bright light conditions and subjects have trouble sleeping. – In constant darkness, people have difficulty waking. Rhythms of Waking and Sleep • Human circadian clock generates a rhythm slightly longer than 24 hours when it has no external cue to set it. • Most people can adjust to 23- or 25- hour day but not to a 22- or 28- hour day. • Bright light late in the day can lengthen the circadian rhythm. Rhythms of Waking and Sleep • Mechanisms of the circadian rhythms include the following: – The Suprachiasmatic nucleus. – Genes that produce certain proteins. – Melatonin levels. Rhythms of Waking and Sleep • The suprachiasmatic nucleus (SCN) is part of the hypothalamus and the main control center of the circadian rhythms of sleep and temperature. – Located above the optic chiasm. – Damage to the SCN results in less consistent body rhythms that are no longer synchronized to environmental patterns of light and dark. Fig. 9-4, p. 269 Rhythms of Waking and Sleep • The SCN is genetically controlled and independently generates the circadian rhythms. • Single cell extracted from the SCN and raised in tissue culture continues to produce action potential in a rhythmic pattern. • Various cells communicate with each other to sharpen the circadian rhythm. Rhythms of Waking and Sleep • Two types of genes are responsible for generating the circadian rhythm. 1. Period - produce proteins called Per. 2. Timeless - produce proteins called Tim. • Per and Tim proteins increase the activity of certain kinds of neurons in the SCN that regulate sleep and waking. • Mutations in the Per gene result in odd circadian rhythms. Fig. 9-5, p. 270 Rhythms of Waking and Sleep • The SCN regulates waking and sleeping by controlling activity levels in other areas of the brain. • The SCN regulates the pineal gland, an endocrine gland located posterior to the thalamus. • The pineal gland secretes melatonin, a hormone that increases sleepiness. Rhythms of Waking and Sleep • Melatonin secretion usually begins 2 to 3 hours before bedtime. • Melatonin feeds back to reset the biological clock through its effects on receptors in the SCN. • Melatonin taken in the afternoon can phaseadvance the internal clock and can be used as a sleep aid. Rhythms of Waking and Sleep • The purpose of the circadian rhythm is to keep our internal workings in phase with the outside world. • Light is critical for periodically resetting our circadian rhythms. • A zeitgeber is a term used to describe any stimulus that resets the circadian rhythms. • Exercise, noise, meals, and temperature are others zeitgebers. Rhythms of Waking and Sleep • Jet lag refers to the disruption of the circadian rhythms due to crossing time zones. – Stems from a mismatch of the internal circadian clock and external time. • Characterized by sleepiness during the day, sleeplessness at night, and impaired concentration. • Traveling west “phase-delays” our circadian rhythms. • Traveling east “phase-advances” our circadian rhythms. Fig. 9-6, p. 272 Rhythms of Waking and Sleep • Light resets the SCN via a small branch of the optic nerve known as the retinohypothalamic path. – Travels directly from the retina to the SCN. • The retinohypothalamic path comes from a special population of ganglion cells that have their own photopigment called melanopsin. – The cells respond directly to light and do not require any input from the rods or cones. Stages of Sleep And Brain Mechanisms • Sleep is a specialized state that serves a variety of important functions including: – conservation of energy. – repair and restoration. – learning and memory consolidation. Stages of Sleep And Brain Mechanisms • The electroencephalograph (EEG) allowed researchers to discover that there are various stages of sleep. • Over the course of about 90 minutes: – a sleeper goes through sleep stages 1, 2, 3, and 4 – then returns through the stages 3 and 2 to a stage called REM. Stages of Sleep And Brain Mechanisms • Alpha waves are present when one begins a state of relaxation. • Stage 1 sleep is when sleep has just begun. – the EEG is dominated by irregular, jagged, low voltage waves. – brain activity begins to decline. Stages of Sleep And Brain Mechanisms • Stage 2 sleep is characterized by the presence of: – Sleep spindles - 12- to 14-Hz waves during a burst that lasts at least half a second. – K-complexes - a sharp high-amplitude negative wave followed by a smaller, slower positive wave. Stages of Sleep And Brain Mechanisms • Stage 3 and stage 4 together constitute slow wave sleep (SWS) and is characterized by: – EEG recording of slow, large amplitude wave. – Slowing of heart rate, breathing rate, and brain activity. – Highly synchronized neuronal activity. Stages of Sleep And Brain Mechanisms • Rapid eye movement sleep (REM) are periods characterized by rapid eye movements during sleep. • Also known as “paradoxical sleep” because it is deep sleep in some ways, but light sleep in other ways. • EEG waves are irregular, low-voltage and fast. • Postural muscles of the body are more relaxed than other stages. Fig. 9-9, p. 276 Stages of Sleep And Brain Mechanisms • Stages other than REM are referred to as non-REM sleep (NREM). • When one falls asleep, they progress through stages 1, 2, 3, and 4 in sequential order. • After about an hour, the person begins to cycle back through the stages from stage 4 to stages 3 and 2 and than REM. • The sequence repeats with each cycle lasting approximately 90 minutes. Stages of Sleep And Brain Mechanisms • Stage 3 and 4 sleep predominate early in the night. – The length of stages 3 and 4 decrease as the night progresses. • REM sleep is predominant later in the night. – Length of the REM stages increases as the night progresses. • REM is strongly associated with dreaming, but people also report dreaming in other stages of sleep. Fig. 9-10, p. 277 Stages of Sleep And Brain Mechanisms • Various brain mechanisms are associated with wakefulness and arousal. • The reticular formation is a part of the midbrain that extends from the medulla to the forebrain and is responsible for arousal. Table 9-1, p. 280 Stages of Sleep And Brain Mechanisms • The pontomesencephalon is a part of the midbrain that contributes to cortical arousal. – Axons extend to the thalamus and basal forebrain which release acetylcholine and glutamate – produce excitatory effects to widespread areas of the cortex. • Stimulation of the pontomesencephalon awakens sleeping individuals and increases alertness in those already awake. Stages of Sleep And Brain Mechanisms • The locus coeruleus is small structure in the pons whose axons release norepinephrine to arouse various areas of the cortex and increase wakefulness. – Usually dormant while asleep. Fig. 9-11, p. 279 Stages of Sleep And Brain Mechanisms • The basal forebrain is an area anterior and dorsal to the hypothalamus containing cells that extend throughout the thalamus and cerebral cortex. • Cells of the basal forebrain release the inhibitory neurotransmitter GABA. • Inhibition provided by GABA is essential for sleep. • Other axons from the basal forebrain release acetylcholine which is excitatory and increases arousal. Fig. 9-12, p. 280 Stages of Sleep And Brain Mechanisms • The hypothalamus contains neurons that release “histamine” to produce widespread excitatory effects throughout the brain. – Anti-histamines produce sleepiness. Stages of Sleep And Brain Mechanisms • Orexin is a peptide neurotransmitter released in a pathway from the lateral nucleus of the hypothalamus highly responsible for the ability to stay awake. – Stimulates acetylcholine-releasing cells in the forebrain and brain stem to increase wakefulness and arousal. Stages of Sleep And Brain Mechanisms • Decreased arousal required for sleep is accomplished via the following ways: 1. Decreasing the temperature of the brain and the body. 2. Decreasing stimulation by finding a quiet environment. 3. Accumulation of adenosine in the brain to inhibit the basal forebrain cells responsible for arousal. – Caffeine blocks adenosine receptors. Stages of Sleep And Brain Mechanisms (cont’d): 4. Accumulation of prostaglandins that accumulate in the body throughout the day to induce sleep. – Prostaglandins stimulate clusters of neurons that inhibit the hypothalamic cells responsible for increased arousal. Stages of Sleep And Brain Mechanisms • During REM sleep: – Activity increases in the pons (triggers the onset of REM sleep), limbic system, parietal cortex and temporal cortex. – Activity decreases in the primary visual cortex, the motor cortex, and the dorsolateral prefrontal cortex. Stages of Sleep And Brain Mechanisms • REM sleep is also associated with a distinctive pattern of high-amplitude electrical potentials known as PGO waves. • Waves of neural activity are detected first in the pons and then in the lateral geniculate of the hypothalamus, and then the occipital cortex. • REM deprivation results in high density of PGO waves when allowed to sleep normally. Fig. 9-13, p. 281 Stages of Sleep And Brain Mechanisms • Cells in the pons send messages to the spinal cord which inhibit motor neurons that control the body’s large muscles. – Prevents motor movement during REM sleep. • REM is also regulated by serotonin and acetylcholine. – Drugs that stimulate Ach receptors quickly move people to REM. – Serotonin interrupts or shortens REM. Stages of Sleep And Brain Mechanisms • Insomnia is a sleep disorder associated with inability to fall asleep or stay asleep. – Results in inadequate sleep. – Caused by a number of factors including noise, stress, pain medication. – Can also be the result of disorders such as epilepsy, Parkinson’s disease, depression, anxiety or other psychiatric conditions. – Dependence on sleeping pills and shifts in the circadian rhythms can also result in insomnia. Fig. 9-15, p. 282 Stages of Sleep And Brain Mechanisms • Sleep apnea is a sleep disorder characterized by the inability to breathe while sleeping for a prolonged period of time. • Consequences include sleepiness during the day, impaired attention, depression, and sometimes heart problems. • Cognitive impairment can result from loss of neurons due to insufficient oxygen levels. • Causes include, genetics, hormones, old age, and deterioration of the brain mechanisms that control breathing and obesity. Stages of Sleep And Brain Mechanisms • Narcolepsy is a sleep disorder characterized by frequent periods of sleepiness. • Four main symptoms include: – Gradual or sudden attack of sleepiness. – Occasional cataplexy - muscle weakness triggered by strong emotions. – Sleep paralysis- inability to move while asleep or waking up. – Hypnagogic hallucinations- dreamlike experiences the person has difficulty distinguishing from reality. Stages of Sleep And Brain Mechanisms (Insomnia cont’d) • Seems to run in families although no gene has been identified. • Caused by lack of hypothalamic cells that produce and release orexin. • Primary treatment is with stimulant drugs which increase wakefulness by enhancing dopamine and norepinephrine activity. Stages of Sleep And Brain Mechanisms • Periodic limb movement disorder is the repeated involuntary movement of the legs and arms while sleeping. – Legs kick once every 20 to 30 seconds for periods of minutes to hours. – Usually occurs during NREM sleep. Stages of Sleep And Brain Mechanisms • REM behavior disorder is associated with vigorous movement during REM sleep. – Usually associated with acting out dreams. – Occurs mostly in the elderly and in older men with brain diseases such as Parkinson’s. – Associated with damage to the pons (inhibit the spinal neurons that control large muscle movements). Stages of Sleep And Brain Mechanisms • “Night terrors” are experiences of intense anxiety from which a person awakens screaming in terror. – Usually occurs in NREM sleep. • “Sleep talking” occurs during both REM and NREM sleep. • “Sleepwalking” runs in families, mostly occurs in young children, and occurs mostly in stage 3 or 4 sleep. Why Sleep? Why REM? Why Dreams? • Functions of sleep include: – Energy conservation. – Restoration of the brain and body. – Memory consolidation. Why Sleep? Why REM? Why Dreams? • The original function of sleep was to probably conserve energy. • Conservation of energy is accomplished via: – Decrease in body temperature of about 1-2 Celsius degrees in mammals. – Decrease in muscle activity. Why Sleep? Why REM? Why Dreams? • Animals also increase their sleep time during food shortages. – sleep is analogous to the hibernation of animals. • Animals sleep habits and are influenced by particular aspects of their life including: – how many hours they spend each day devoted to looking for food. – Safety from predators while they sleep • Examples: Sleep patterns of dolphins, migratory birds, and swifts. Fig. 9-17, p. 287 Why Sleep? Why REM? Why Dreams? • Sleep enables restorative processes in the brain to occur. – Proteins are rebuilt. – Energy supplies are replenished. • Moderate sleep deprivation results in impaired concentration, irritability, hallucinations, tremors, unpleasent mood, and decreased responses of the immune system. Why Sleep? Why REM? Why Dreams? • People vary in their need for sleep. – Most sleep about 8 hours. • Prolonged sleep deprivation in laboratory animals results in: – Increased metabolic rate, appetite and body temperature. – Immune system failure and decrease in brain activity. Why Sleep? Why REM? Why Dreams? • Sleep also plays an important role in enhancing learning and strengthening memory. – Performance on a newly learned task is often better the next day if adequate sleep is achieved during the night. • Increased brain activity occurs in the area of the brain activated by a newly learned task while one is asleep. – Activity also correlates with improvement in activity seen the following day. Why Sleep? Why REM? Why Dreams? • Humans spend one-third of their life asleep. • One-fifth of sleep time is spent in REM. • Species vary in amount of sleep time spent in REM. – Percentage of REM sleep is positively correlated with the total amount of sleep in most animals. • Among humans, those who get the most sleep have the highest percentage of REM. Fig. 9-18, p. 289 Why Sleep? Why REM? Why Dreams? • REM deprivation results in the following: – Increased attempts of the brain/ body for REM sleep throughout the night. – Increased time spent in REM when no longer REM deprived. • Subjects deprived of REM for 4 to 7 nights increased REM by 50% when no longer REM deprived. Why Sleep? Why REM? Why Dreams? • Research is inconclusive regarding the exact functions of REM. • During REM: – The brain may discard useless connections – Learned motor skills may be consolidated. • Maurice (1998) suggests the function of REM is simply to shake the eyeballs back and forth to provide sufficient oxygen to the corneas. Why Sleep? Why REM? Why Dreams? • Biological research on dreaming is complicated by the fact that subjects can not often accurately remember what was dreamt. • Two biological theories of dreaming include: 1. The activation-synthesis hypothesis. 2. The clinico-anatomical hypothesis. Why Sleep? Why REM? Why Dreams? • The activation-synthesis hypothesis suggests dreams begin with spontaneous activity in the pons which activates many parts of the cortex. – The cortex synthesizes a story from the pattern of activation. – Normal sensory information cannot compete with the self-generated stimulation and hallucinations result. Why Sleep? Why REM? Why Dreams? • Input from the pons activates the amygdala giving the dream an emotional content. • Because much of the prefrontal cortex is inactive during PGO waves, memory of dreams is weak. – Also explains sudden scene changes that occur in dreams. Why Sleep? Why REM? Why Dreams? • The clinico-anatomical hypothesis places less emphasis on the pons, PGO waves, or even REM sleep. – Suggests that dreams are similar to thinking, just under unusual circumstances. • Similar to the activation synthesis hypothesis in that dreams begin with arousing stimuli that are generated within the brain. – Stimulation is combined with recent memories and any information the brain is receiving from the senses. Why Sleep? Why REM? Why Dreams? • Since the brain is getting little information from the sense organs, images are generated without constraints or interference. • Arousal can not lead to action as the primary motor cortex and the motor neurons of the spinal cord are suppressed. • Activity in the prefrontal cortex is suppressed which impairs working memory during dreaming. Why Sleep? Why REM? Why Dreams? • Activity is high in the inferior part of the parietal cortex, an area important for visualspatial perception. – Patients with damage report problems with binding body sensations with vision and have no dreams. – Activity is also high in areas outside of V1, accounting for the visual imagery of dreams. Why Sleep? Why REM? Why Dreams? • Activity is high in the hypothalamus and amygdala which accounts for the emotional and motivational content of dreams. • Either internal or external stimulation activates parts of the parietal, occipital, and temporal cortex. • Lack of sensory input from V1 and no criticism from the prefrontal cortex creates the hallucinatory perceptions.