Chapter 9 Wakefulness and Sleep

Name: Chapter 9 Wakefulness and Sleep
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Description: Chapter 9 Wakefulness and Sleep

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.

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 Figure 9.2: Mean rectal temperatures for nine adults.
Body temperature reaches its low for the day about 2 hours after sleep onset; it reaches its peak about 6 hours before sleep onset. (Source: From “Sleep-onset insomniacs have delayed temperature rhythms,” by M. Morris, L. Lack, and D. Dawson, Sleep, 1990, 13, 1–14. Reprinted by permission) Fig. 9-2, p. 267

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.

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.

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.

Mechanisms of the circadian rhythms include the following: The Suprachiasmatic nucleus. Genes that produce certain proteins. Melatonin levels.

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.

Figure 9.4: The suprachiasmatic nucleus (SCN) of rats and humans.
The SCN is located at the base of the brain, just above the optic chiasm, which has torn off in these coronal sections through the plane of the anterior hypothalamus. Each rat was injected with radioactive 2-deoxyglucose, which is absorbed by the most active neurons. A high level of absorption of this chemical produces a dark appearance on the slide. Note that the level of activity in SCN neurons is much higher in section (a), in which the rat was injected during the day, than it is in section (b), in which the rat received the injection at night. (c) A sagittal section through a human brain showing the location of the SCN and the pineal gland. (Source: (a) and (b) W. J. Schwartz & Gainer, 1977) Fig. 9-4, p. 269

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.

Two types of genes are responsible for generating the circadian rhythm. Period - produce proteins called Per. 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.

Figure 9.5: Feedback between proteins and genes to control sleepiness.
In fruit flies (Drosophila), the Tim and Per proteins accumulate during the day. When they reach a high level, they induce sleepiness and shut off the genes that produce them. When their levels decline sufficiently, wakefulness returns and so does the gene activity. A pulse of light during the night breaks down the Tim protein, thus increasing wakefulness and resetting the circadian rhythm. Fig. 9-5, p. 270

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.

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 phase-advance the internal clock and can be used as a sleep aid.

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.

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.

Figure 9.6: Jet lag. Eastern time is later than western time. People who travel six time zones east fall asleep on the plane and then must awaken when it is morning at their destination but still night back home. Fig. 9-6, p. 272

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.

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.

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.

Stage 2 sleep is characterized by the presence of: Sleep spindles 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.

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.

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.

Figure 9.9: Polysomnograph records from a male college student.
A polysomnograph includes records of EEG, eye movements, and sometimes other data, such as muscle tension or head movements. For each of these records, the top line is the EEG from one electrode on the scalp; the middle line is a record of eye movements; and the bottom line is a time marker, indicating 1-second units. Note the abundance of slow waves in stages 3 and 4. (Source: Records provided by T. E. LeVere) Fig. 9-9, p. 276

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.

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.

Figure 9.10: Sequence of sleep stages on three representative nights.
Columns indicate awake (A) and sleep stages 2, 3, 4, and REM. Deflections in the line at the bottom of each chart indicate shifts in body position. Note that stage 4 sleep occurs mostly in the early part of the night’s sleep, whereas REM sleep becomes more prevalent toward the end. (Source: Based on Dement & Kleitman, 1957a) Fig. 9-10, p. 277

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

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.

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.

Figure 9.11: Brain mechanisms of sleeping and waking.
Green arrows indicate excitatory connections; red arrows indicate inhibitory connections. Neurotransmitters are indicated where they are known. Although adenosine is shown as a small arrow, it is a metabolic product that builds up in the area, not something released by axons. (Source: Based on Lin, Hou, Sakai, & Jouvet, 1996; Robbins & Everitt, 1995; and Szymusiak, 1995) Fig. 9-11, p. 279

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 Figure 9.12: Basal forebrain.
The basal forebrain is the source of many excitatory axons (releasing acetylcholine) and inhibitory axons (releasing GABA) that regulate arousal of the cerebral cortex. Fig. 9-12, p. 280

The hypothalamus contains neurons that release “histamine” to produce widespread excitatory effects throughout the brain. Anti-histamines produce sleepiness.

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.

Decreased arousal required for sleep is accomplished via the following ways: Decreasing the temperature of the brain and the body. Decreasing stimulation by finding a quiet environment. Accumulation of adenosine in the brain to inhibit the basal forebrain cells responsible for arousal. Caffeine blocks adenosine receptors.

(cont’d): 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.

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.

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 Figure 9.13: PGO waves.
PGO waves start in the pons (P) and then show up in the lateral geniculate (G) and the occipital cortex (O). Each PGO wave is synchronized with an eye movement in REM sleep. Fig. 9-13, p. 281

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.

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 Figure 9.15: Insomnia and circadian rhythms.
A delay in the circadian rhythm of body temperature is associated with onset insomnia; an advance, with termination insomnia. Fig. 9-15, p. 282

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.

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.

(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.

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.

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).

“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.

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.

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.

Figure 9.17: Hours of sleep per day for various animal species.
Generally, predators and others that are safe when they sleep tend to sleep a great deal; animals in danger of being attacked while they sleep spend less time asleep. Fig. 9-17, p. 287

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.

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.

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.

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.

Figure 9.18: Time spent by people of different ages in waking, REM sleep, and NREM sleep.
REM sleep occupies about 8 hours a day in newborns but less than 2 hours in most adults. The sleep of infants is not quite like that of adults, however, and the criteria for identifying REM sleep are not the same. (Source: From “Ontogenetic development of human sleep-dream cycle,” by H. P. Roffwarg, J. N. Muzio, and W. C. Dement, Science, 152, 1966, 604–609. Copyright 1966 AAAS. Reprinted by permission.) Fig. 9-18, p. 289

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.

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.

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: The activation-synthesis hypothesis. The clinico-anatomical hypothesis.

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.

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.

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.

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.

Activity is high in the inferior part of the parietal cortex, an area important for visual-spatial 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.

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.

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