Sleep, Dreaming, and Circadian Rhythms

Question 1

three standard psychophysiological bases for defining the stages of sleep.

Answer 1

Subsequently, the electroencephalogram (EEG), the electrooculogram (EOG), and the neck electromyogram (EMG)

Question 2

stages of sleep

Answer 2

first: After the eyes are shut and a person prepares to go to sleep, alpha waves—waxing and waning bursts of 8- to 12-Hz EEG waves—begin to punctuate the low-voltage, high-frequency waves of alert wakefulness.
1. initial stage 1 sleep, low-voltage, high-frequency signal that is similar to, but slower than, that of alert wakefulness.NREM 1
2.. stage 2 sleep, higher amplitude and lower frequency and K complexes and sleep spindles (large negative and positive wave) NREM 2
3. stage 3 of sleep, delta waves (largest and slowest). people stay in stage 3 for a longer time and then go to.. NREM 3 or slow wave sleep (SWS)
4. emergent stage 1 –> rapid eye movements (REMs) and by a loss of tone in the muscles of the body core. veel cerebral activity (zoals je ook hebt als je wakker bent). ANS activity (high bp, pulse etc..) vaak erectie en spier samentrekkingen.

later in de nacht steeds meer in REM en minder in stage 3. 90 min cyclus en soms wakker.

Question 3

some common beliefs about dreaming

Answer 3

• external stimuli are sometimes incorporated in dreams, some stimuli more than others (water and pressure on limbs)
• dream duration –> Current research on dream duration supports the notion that dreams run slightly slower than real time. For example, physical movement while in a dream can take up to 40% longer than in a waking state.
• people have penile erections during sleep, not only when draming about sex
• sleeptalking can happen in any stage but ofter during transition to wakefulness and sleepwalking mostly in SWS, never in REM bv muscles are relaxed.

Question 4

dreams and REM

Answer 4

you can also dream in NREM, same kind of dreams, mostly later in the night. REM is not so associated with dreams.

Question 5

2 key findings about the content of a dream

Answer 5

1. there is a general consensus that dream content is influenced by what we have experienced in the prior period of wakefulness )—even the most mundane of experiences, like taking out the garbage, can enter a subsequent dream.
2. The amount of anxiety experienced prior to a bout of dreaming affects the emotional content of dreams.

Question 6

3 different theories of why we dream

Answer 6

1. HOBSON’S ACTIVATION-SYNTHESIS HYPOTHESIS. = de info die naar de cortex gaan tijdens het slapen is random en een droom is de cortexs manier om sense van die random signalen te maken.
2. REVONSUO’S EVOLUTIONARY THEORY OF DREAMS. = we dream to simulate threatening events, such as physical attack, threats to social relationships, or threats to one’s livelihood, and that such simulation allows us to better predict and respond to such threats when we are awake.
3. HOBSON’S PROTOCONSCIOUSNESS HYPOTHESIS. = hij geloofde ook dat het een evolutionair voordeel heeft maar niet alleen voor threatening siatuaties maar voor elke situatie. –> dreaming is a training mechanism, with each dream repre- senting a virtual real-life scenario. the term “protoconsciousness”: a virtual prototype of our conscious experiences.

Question 7

hersengebieden involved in dromen

Answer 7

stopzetten dromen:
- bilateral lesions of the temporo-parieto junction and
- bilateral lesions of the medial prefrontal cortex and
- lesions of secondary visual cortex in medial occipital lobe lead to loss of visual imagery in dreams.

die gebieden allemaal verhoogde activiteit tijdens REM. temporo-parieto junction ook bij NREM dreaming, dus bij allebei

Question 8

recuperation theories of sleep

Answer 8

being awake disrupts the homeostasis (internal physiological stability) of the body in some way and sleep is required to restore it.

the three most common recuperation theories of sleep are that the function of sleep is to (1) restore energy levels that decline during wakefulness, (2) clear toxins (e.g., beta-amyloid—see Chapter 10) from the brain and other tissues that accumu- late during wakefulness, or (3) restore the synaptic plasticity that might dissipate during wakefulness

Question 9

adaptation theories of sleep

Answer 9

sleep is not a reaction to the disruptive effects of being awake but the result of an internal 24-hour timing mechanism—that is, we humans are programmed to sleep at night regardless of what happens to us during the day. more focus on when we sleep thean the function of sleep.

their strong motivation to sleep at night evolved to conserve their energy resources, make them less susceptible to mishaps in the dark (e.g., predation), and to carry out certain brain functions that aren’t possible during wakefulness.

Adaptation theories suggest that sleep is like reproductive behavior in the sense that we are highly motivated to engage in it, but we don’t need it to stay healthy.

Question 10

consequenties van sleepdeprivation

Answer 10

1. more sleepy
2. perform poorly on tests of substanied attention
3. negative affect on tests of mood

tests of logical deduction or critical thinking, are tests proved to be largely immune to disruption. In contrast, performance on tests of executive function proved to be more susceptible to disruption by sleep loss

Question 10

default theory of REM sleep

Answer 10

difficult to stay continuously in NREM sleep, so the brain periodically switches to one of two other states. If there are any immediate bodily needs to be taken care of (e.g., the need for food or water), the brain switches to wakefulness; if there are no immediate needs, it switches to REM sleep. According to the default theory, REM sleep is more adaptive than wakefulness when there are no immediate bodily needs.

mensen werken 15 min wakker gehouden voor elke gemiste REM sleep fase en ze waren niet moe de dag daarna. In other words, there seemed to be no need for REM sleep if periods of wakefulness were sub- stituted for it. This finding is consistent with the finding that as antidepressants reduce REM sleep, the number of nighttime awakenings increases

Question 11

circadian rythm and zeitgeber (time givers) (temporals cues like light) without zeitgebers: free-running rhythms, and their duration is called the free-running period.

Answer 11

Free-running periods vary in length from individual to indi- vidual, are of relatively constant duration within a given individual, and are usually longer than 24 hours—about 24.2 hours is typical in humans living under constant mod- erate illumination. It seems that we all have an internal biological clock that habitually runs a little slow unless it is entrained by time-related cues in the environment.

Question 12

internal desynchronization

Answer 12

when subjects are housed in constant laboratory environments, their sleep–wake and body tem- perature cycles sometimes break away from one another. This phenomenon is called internal desynchronization (see Daan, Honma & Honma, 2013). For example, in one human volunteer, the free-running periods of both the sleep–wake and body temperature cycles were initially 25.7 hours; then, for some unknown reason, there was an increase in the free-running period of the sleep–wake cycle to 33.4 hours and a decrease in the free-running period of the body temperature cycle to 25.1 hours. The potential for the simultaneous existence of two different free-running periods was the first evidence that there is more than one circadian timing mechanism, and that sleep is not caus- ally related to the decreases in body temperature normally associated with it.

Question 13

brain area involved in carcadian rythm

Answer 13

suprachiasmatic nuclei (SCN) of the medial hypothalamus

• Under certain conditions, bilateral SCN lesions have been shown to leave some circadian rhythms unaf- fected while abolishing others.
• Bilateral SCN lesions do not eliminate the ability of all environmental stimuli to entrain circadian rhythms (see Saper, 2013); for example, SCN lesions can block entrainment by light but not by regular food or water availability (see Mistlberger, 2011).
• Just like suprachiasmatic neurons, cells from other parts of the body often display free-running circadian cycles of activity when maintained in tissue culture.

retinohypothalamic tracts mediate the ability of light to entrain circadian rhythms, –> retinal ganglion cells with distinctive functional properties, Their photopigment is melanopsin

Question 14

genetics of circadian rhytms

Answer 14

tau gene involved in circadian rhytm

Question 15

brain areas involved in sleep discovered by brain stem transections inncats

Answer 15

cerveau isolé preparation: Bremer severed the brain stems of cats between their inferior colliculi and superior colliculi in order to disconnect their forebrains from ascending sensory input (surgical preparation) –> Bremer found that the cortical EEG of the isolated cat forebrains was indicative of almost continuous slow-wave sleep. Only when strong visual or olfactory stimuli were presented (the cerveau isolé has intact visual and olfactory input) could the continuous high-amplitude, slow-wave activity be changed to a desynchronized EEG—a low- amplitude, high-frequency EEG. However, this arousing effect barely outlasted the stimuli.

ncéphale isolé preparation –> showed that the structure for maintaining wakefulness was located in the brain stem between the sections

structure for maintaining wakefulness: brainstem (reticular formation) –> reticular activating system

• posterior and anterior hypothalamus
• structure for maintaining wakefulness: brainstem (reticular formation) –> reticular activating system

Question 16

drugs that affect sleep

Answer 16

• hypnotic drugs
  –> BENZO
  –> imidazopyridines (zonder sinde effects van benzo maar bleek niet beter (zolpidem))
  –> 5-HTP (raphe nuclei speelt een rol in slaap en deze serotonergic drugs zou daar invloed op kunnen hebben maar bij mensen helpt het niet bij insomnia
• antihypnotic drugs
  –> cocaine-derived stimulants, amphetamine-derived stimulants, and tricyclic antidepressants.
  –> The drugs in these three classes seem to promote wake- fulness by boosting the activity of catecholamines (nor- epinephrine, epinephrine, and dopamine)—by increasing their release into synapses, by blocking their reuptake from synapses, or both.
• melatonin, hormone gesynthetiseerd van nt serotonin in the pineal gland
  –> beter beschreven als chronobiotic (a substance that adjusts the timing of internal biological rhythms) than as a soporific (sleep-promoting)

Question 17

many cases of insomnia are

Answer 17

iatrogenic (physician-created)— in large part because sleeping pills (e.g., benzodiazepines), which are usually prescribed by physicians, are a major cause of insomnia

Question 18

2 types of sleep apnea

Answer 18

(1) obstructive sleep apnea results from obstruction of the respiratory passages by muscle spasms or atonia (lack of muscle tone) and often occurs in individuals who are vigorous snorers

(2) central sleep apnea results from the failure of the central nervous system to stimulate respiration

Question 19

2 specific causes of insomnia

Answer 19

• Periodic limb movement disorder:
  is characterized by periodic, involuntary movements of the limbs, often involving twitches of the legs during sleep. Most patients suffering from this disorder complain of poor sleep and daytime sleepiness but are unaware of the nature of their problem.

In contrast, people with
- restless legs syndrome are all too aware of their problem. They complain of a hard- to-describe tension or uneasiness in their legs that keeps them from falling asleep (see Lai et al., 2017). Once estab- lished, both of these disorders are chronic (see Ondo, 2019; Stevens, 2015). There are no effective treatments for these disorders, although l-dopa (see Chapter 10) can help some patients (see Ondo, 2019).

Question 20

characteristics of narcolepse

Answer 20

• daytime sleep attacks
• cataplexy (recurring losses of muscle tone during wakefulness, often triggered by an emotional experience)
• sleep paralysis
• hypnagogic hallucinations

orexin (hypocretin) A en B hebben misschien iets te doen met narcolepsy Several studies have documented reduced levels of orexin in the cerebrospinal fluid of individuals living with narcolepsy and in the brains of deceased individuals who had narcolepsy (see Nishino & Kanbayashi, 2005). Also, the number of orexin-releasing neurons has been found to be reduced in the brains of persons with narcolepsy (see Mahoney et al., 2019; Shan, Dauvilliers, & Siegel, 2015). One popular explanation for the loss of orexin-releasing neurons in narcolepsy is that it is the result of an autoimmune response

Orexin is syn- thesized by neurons in the region of the hypothalamus that has been linked to the promotion of wakefulness: the pos- terior hypothalamus. The orexin-producing neurons project diffusely throughout the brain, but they show many con- nections with neurons in the other wakefulness-promoting area of the brain: the reticular formation.

The antihypnotic stimulant modafinil has been shown to be effective in the treatment of some cases of nar- colepsy, and certain antidepressants can be effective against cataplexy (see Scammell, 2015).

Question 21

rem related disorders

Answer 21

narcolepsy can be seen as a REMRD

REM-sleeo behvior disorder is rem without coremuscle atonia (acting out your dreams) a lot in parkinson

Question 22

Most mammals and human infants display polyphasic sleep cycles; that is, they regularly sleep more than once per day. In contrast, most adult humans display monophasic sleep cycles; that is, they sleep once per day.