1. Chapter 9 Wakefulness and Sleep

2. Rhythms of Waking 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.

3. Rhythms of Waking and Sleep All animals produce endogenous circadian rhythms, internal mechanisms that operate on an approximately 24 hour cycle. Animals generate endogenous 24 hour cycles of wakefulness and sleep. –Also regulates the frequency of eating and drinking, body temperature, secretion of hormones, urination, and sensitivity to drugs.

4. Rhythms of Waking and Sleep 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.

5. Rhythms of Waking and Sleep The purpose of the circadian rhythm is to keep our internal workings in phase with the outside world. Human circadian clock generates a rhythm slightly longer than 24 hours when it has no external cue to set it. Resetting our circadian rhythms is sometimes necessary.

6. Rhythms of Waking and Sleep Free-running rhythm is a rhythm that occurs when no stimuli resets it. A zeitgeber is a term used to describe any stimulus that resets the circadian rhythms. Light is the primary one. Exercise, noise, meals, and temperature are others zeitgebers.

7. 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.

9. Rhythms of Waking and Sleep Circadian rhythms remain consistent despite lack of environmental cues indicating the time of day Most people can adjust to 23- or 25- hour day but not to a 22- or 28- hour day. People who engage in shift work often fail to adjust completely.

10. Rhythms of Waking and Sleep Mechanisms of the circadian rhythms include the following: –The Suprachiasmatic nucleus –Genes that produce certain proteins –Melatonin levels

11. 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.

13. Rhythms of Waking and Sleep The SCN generates circadian rhythms in a genetically controlled, unlearned manner. 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.

14. 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.

16. 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.

18. 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.

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

20. Stages of Sleep And Brain Mechanisms Sleep is a state that the brain actively produces. Characterized by a moderate decrease in brain activity and decreased response to stimuli. Sleep differs from the following states: –Coma –Vegetative state –Minimally conscious state –Brain death

21. Stages of Sleep And Brain Mechanisms Coma – extended period of unconsciousness caused by head trauma, stroke, or disease characterized by low brain activity that remains fairly steady –Person shows little response to stimuli Vegetative state – person alternates between periods of sleep and moderate arousal but no awareness of surrounding –Some autonomic arousal to painful stimulus –No purposeful activity/ response to speech

22. Stages of Sleep And Brain Mechanisms Minimally conscious state - one stage higher than a vegetative state marked by occasional brief periods of purposeful action and limited speech comprehension Brain death - no sign of brain activity and no response to any stimulus

23. Stages of Sleep And Brain Mechanisms The electroencephalograph (EEG) allowed researchers to discover that there are various stages of sleep. Allows researchers to compare brain activity at different times during sleep. A polysomnograph is a combination of EEG and eye-movement records

25. 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.

26. 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-complex - a sharp high-amplitude negative wave followed by a smaller, slower positive wave.

27. 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.

28. Stages of Sleep And Brain Mechanisms Rapid eye movement sleep (REM) are periods characterized by rapid eye movements during sleep. Also know as paradoxical sleep 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.

30. 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.

31. 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.

33. 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.

34. 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.

35. 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.

37. StructureNeurotransmitter(s) it releases Effects on Behavior PontomesencephalonAcetylcholine, glutamateIncreases cortical arousal Locus coeruleusNorepinephrineIncreases information storage during wakefulness; suppresses REM sleep Basal forebrain Excitatory cellsAcetylcholineExcites thalamus and cortex; increases learning, attention; shifts sleep from NREM to REM Inhibitory cellsGABAInhibits thalamus and cortex Hypothalamus (parts)HistamineIncreases arousal (parts)OrexinMaintains wakefulness Dorsal raphe and ponsSerotoninInterrupts REM sleep

38. 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.

39. 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.

40. 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 basal forebrain to stimulate neurons responsible for wakefulness and arousal. –The basal forebrain is an area just anterior and dorsal to the hypothalamus

41. Stages of Sleep And Brain Mechanisms Functions of the inhibitory neurotransmitter GABA are also important: 1.Decreasing the temperature and metabolic rate 2.Decreasing stimulation of neurons.

42. Stages of Sleep And Brain Mechanisms During REM sleep: –Activity increases in the pons (triggers on set of REM sleep) and limbic system (emotional systems), parietal cortex and temporal cortex. –Activity in the pons triggers onset of REM sleep –Activity decreases in the primary visual cortex, the motor cortex, and the dorsolateral prefrontal cortex.

43. 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.

45. 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 REM.

47. Stages of Sleep And Brain Mechanisms Insomnia is a sleep disorder associated with 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.

49. 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 may 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.

51. 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.

52. 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.

53. 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.

54. 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).

55. 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.

56. Why Sleep? Why REM? Why Dreams? Functions of sleep include: –Energy conservation. –Restoration of the brain and body. –Memory consolidation.

57. 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.

58. 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.

60. Why Sleep? Why REM? Why Dreams? Sleep enables restorative processes: –Proteins rebuilt in the brain –Energy supplies replenished Moderate sleep deprivation results in impaired concentration, irritability, hallucinations, tremors, unpleasant mood, and decreased immune system functioning. Caffeine increases arousal by blocking the receptors for adenosine (accumulate during wakefulness and increase drowsiness)

61. 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.

62. 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.

63. 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.

65. 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.

66. 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.

67. 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.

68. 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.

69. 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.

70. Why Sleep? Why REM? Why Dreams? 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.

71. 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.