Sleep

Question 1

Sleep stages and brain activity

Answer 1

• Electroencephalogram (EEG): electrodes attached to the scalp record electrical activity of the brain
  
  • Electromyogram (EMG): electrodes attached to the chin monitor muscle activity
    Electro-oculogram (EOG): monitors eye movements

Question 2

Brain activity during sleep- stage 1

Answer 2

○ Slower waves than that of alert wakefulness but still low-voltage and high-frequency (alpha: 8 to 12 Hz)
As we progress from Stage 1 sleep through Stages 2, 3 and 4, there is a gradual increase in voltage and decrease in frequency.
- Initial stage 1:
○ First period of stage 1, not marked by any major EMG or EOG activity changes.
- Emergent stage 1:
○ Subsequent stage 1 periods, marked by loss of muscle tone and characterised by rapid eye movements (REMs).
All other stages of sleep are known as non-REM (NREM) sleep.

Question 3

brain activity duing sleep- stage 2

Answer 3

○ Increase in theta wave activity (4 to 7 Hz) and body goes into a stage of deep relaxation.
○ Theta waves are interrupted by brief bursts of activity known as sleep spindles (high-frequency).
○ Spindles are 1-2 second bursts of 12- to 14- Hz waves.
A K-complex can also be observed - a very high amplitude pattern of brain activity.

Question 4

brain activity during sleep- stage 3

Answer 4

Deep sleep or slow-wave sleep is defined by the occasional presence of delta waves - largest and slowest waves (1 to 2 Hz)

Question 5

brain activity during sleep- stage 4

Answer 5

○ Predominance of delta waves - we stay in Stage 4 for a time before retreating back through sleep stages to stage 1.
Stages 3 and 4 together are referred to as slow-wave sleep (SWS).
After stage 4, we return to stage 1 but sleep activity is not the same.

Question 6

REM sleep

Answer 6

○ During REM we observe high brain activity and lack of muscle tone.
REM sleep is thought to be the physiological correlate of dreaming as 80% of dream recalls happen during awakenings from REM sleep - while only 7% arise from NREM (not full narratives but isolated experiences- e.g. “I was falling”).

Question 7

sleep and age

Answer 7

• Proportion of REM sleep does not change after adulthood
  Proportion of NREM sleep declines continuously → elderly individuals would show a decrease in slow-wave sleep

Question 8

sleep theories

Answer 8

• Two types of theories for sleep have been proposed:
  
  • Recuperation theories
    ○ The main principle behind recuperation theories is that being awake disrupts the homeostasis (internal physiological stability) of the body and sleep is required to restore it.
  • Adaptation theories
    Sleep is the result of an internal 24-hour timing mechanism. Humans have evolved to sleep at night because sleep protects us from accident and predation during the night.

Question 9

what happens when we don’t sleep

Answer 9

• tiredness, irritability, frequent infections, inability to tolerate stress, deteriorated memory

Question 10

predictions of recuperation theories about sleep deprivation

Answer 10

• Because this theory is based on the premise that sleep is a response to the accumulation of some debilitating effect of wakefulness, three predictions are made about the effects of sleep deprivation:
• Long periods of wakefulness will produce physiological and behavioural disturbances
• These disturbances will grow steadily worse as the deprivation continues
• After the period of deprivation has ended, much of the missed sleep will be regained

Question 11

sleep deprivation case studies: sleep deprived students (Kleiman, 1963)

Answer 11

• Most students that were deprived of sleep experienced the same effects. On the first night they read or studied with little difficulty after 3am and then experienced an attack of sleepiness.
• The next day the students were alert as long as they remained active, but during the night reading or studying was next to impossible.
  This daily cycle continued for the next days with students being relatively alert when active and having severe sleepiness during the later hours.

Question 12

sleep deprivation case studies: the case of Randy Gardner (Dement, 1978)

Answer 12

• Randy and his classmates wanted to break the world record of 260 hours (~11 days) of wakefulness.
• He did manage to stay awake until the 11th day (264 hours) and then he slept for 14 hours (a Guinness World Record back then).
• He experienced significant deficits in concentration, motivation, perception, and higher mental processes during his sleep deprivation. However, he recovered normal cognitive functions after a few nights of sleep.
  After the first night he went back to his 8-hour sleep schedule which was surprising - he didn’t need to ‘catch up’ on lost sleep.

Question 13

REM sleep deprivation

Answer 13

• REM-sleep deprivation has two consistent effects:
  
  • Participants display a REM rebound, that is they have more than their usual amount of REM sleep for the first two or three nights.
  • With each successive night of deprivation, there is a greater tendency for participants to initiate REM sequences. As REM-sleep deprivation proceeds, participants have to be awakened more and more frequently to keep them from accumulating significant amounts of REM sleep.
    For example, during the first night of REM-sleep deprivation in one experiment (Webb & Agnew, 1967), participants had to be awakened 17 times to keep them from having extended periods of REM sleep; but during the seventh night of deprivation, they had to be awakened 67 times.

Question 14

function of rem sleep

Answer 14

• The fact that REM sleep is compensated for after deprivation suggests that it is regulated separately from slow-wave sleep and may serve a special function.
• One theory suggests that REM sleep is important for memory consolidation. However, there have been conflicting findings (inconclusive evidence).
  According to the default theory of REM sleep, it is 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., food or water), the brain switches to wakefulness; if there are no immediate needs, it switches to REM sleep.

Question 15

REM sleep and dreaming

Answer 15

• If awakened during NREM and ask people if they were dreaming they’ll probably say “no”
• If you question more carefully they’ll report the presence of some image or emotion (e.g., I was falling)
• On the other hand dreams of REM sleep tend to be narrative in form with a story like progression of events
• Initially it was assumed that dreams only happened during REM sleep.
  Even when reporting dreaming when awakened during NREM, the dreams were attributed to remembering previous dreams that happened during REM.

Question 16

why do we dream?

Answer 16

• Early civilisations – a medium between earthly world and the Gods
• Greeks and Romans – dreams had prophetic powers
• Numerous theories have been proposed to explain the mystery behind dreams
• Psychological theories:
  
  • Freud and Jung
  • Threat-simulation theory
  • Expectation Fulfilment theory
• Neurobiological theories:
  
  • Activation-synthesis theory
    Continual activation theory

Question 17

psychological theories of dreaming

Answer 17

• Freud believed that dreams are triggered by unacceptable repressed wishes, often of a sexual nature. He argued that the dreams we experience (our manifest dreams) are merely disguised versions of our real dreams (our latent dreams). There is no convincing evidence for this theory.
• According to the threat-simulation theory, dreaming can be thought of as an ancient biological defence mechanism that prepares us for dealing with potential threatening events. When certain threats are rehearsed during our dreams the neurocognitive mechanisms for threat perception and avoidance can be trained and this can provide an evolutionary advantage.
• The expectation-fulfilment theory suggests that dreaming allows emotional arousals that haven’t been expressed during the day to be discharged and that can free up space in the brain to deal with tomorrow’s emotional cues.
  In effect, the expectation is fulfilled (the action is “completed”) in a metaphorical form so that a false memory is not created (recollection of an event that actually did not occur..). This theory explains why dreams are usually forgotten immediately afterwards.

Question 18

neurobiological theories of dreaming

Answer 18

• The activation-synthesis theory (Hobson, 1989) proposes that the information supplied to the cortex during REM sleep is largely random and that the resulting dream is the cortex’s effort to make sense of these random signals. Basically, we construct dream stories when we wake up to give sense to content.
  The continual-activation theory (Zhang, 2005) states that the function of sleep is to process, encode, and transfer data from short-term memory to long-term memory through a process called consolidation. It also posits that NREM sleep processes conscious-related memory (declarative memory) and REM sleep processes the unconscious-related memory (procedural memory).

Question 19

long term memory definitions

Answer 19

• Procedural memory: how to perform certain actions (learned; e.g. riding a bike)
  Declarative memory: Recalling facts or events (explicit; e.g. someone’s birthday or what you did three years ago during a summer vacation)

Question 20

brain areas involved in sleep regulation- hypothalamus

Answer 20

• The two key brain areas involved in sleep regulation were discovered during World War I by Constantin von Economo - a Viennese neurologist.
• He examined victims of a serious viral infection - encephalitis lethargica - which led to the deaths of about 1.5 million people in a 1915-1926 epidemic.
• The majority of patients slept for more than 20 hours per day, arising only to eat and drink. Their cognitive function was intact, but they would soon return to sleep.
• A minority of patients had difficulty sleeping.
• He found that deceased victims with excessive sleep symptoms had damage in the posterior hypothalamus, while victims with the opposite problem had damage in the anterior hypothalamus.
  His findings and assumptions about the hypothalamus were later confirmed by lesion and animal experimental studies.

Question 21

brain areas involved in sleep regulation- reticular formation

Answer 21

• In 1936, Bremer experimented in cats, severing their brain stem in several areas:
• Between the inferior and superior colliculi to disconnect their forebrains from ascending sensory input (“cerveau isolé”, or isolated forebrain)→ continuous SWS
• Transection (cutting through) caudal to the colliculi (“encéphale isolé”, or isolated brain) cutting most of the same sensory fibers → normal sleep cycle
  This suggested that the structure involved in wakefulness was located somewhere in the brainstem between these two transections.
• Two more findings suggested that this structure was the reticular formation:
• Partial transections at the cerveau isolé level disrupted normal sleep-wake cycles of cortical EEG only when they severed the reticular formation core of the brain stem.
• Electrical stimulation of the reticular formation of sleeping cats awakened them
• Based on these four findings Moruzzi and Magoun (1949) proposed that low levels of activity in the reticular formation produce sleep and that high levels produce wakefulness → reticular formation known as the reticular activating system.
• Similarities between REM and wakefulness suggest that the same brain area might be involved in controlling both.
• REM sleep is controlled by nuclei in the caudal reticular formation, each controlling a different aspect of REM:
  
  • Atonia (loss of muscle tone)
  • Rapid eye movements
    Cardiorespiratory changes

Question 22

neurochemical control of sleep

Answer 22

• Sleep is regulated – suggesting a monitoring mechanism
• Do sleep-promoting substances or wakefulness promoting substances exist?
• Substances do not appear to circulate in the blood
• Controlled by chemicals that are produced and act within the brain
• Because REM and NREM sleep are regulated independently there might be two substance
• The amount and timing of sleep is regulated by two major factors:
• Homeostatic drive (the body’s need for sleep)
• Circadian rhythm (the body’s biological clock for the sleep-wake cycle)
• The control of sleep can also be allostatic in nature
• → Under some circumstances it is important to stay awake, as for example when reacting to stressful events in the environment (danger, lack of water) → override homeostatic control
  Since sleep can be regulated, are there sleep-promoting substances or wakefulness promoting substances in the brain?

Question 23

role of adenosine in sleep

Answer 23

• Adenosine is a substance that accumulates with waking hours and drives the pressure to sleep.
• Caffeine promotes wakefulness by acting as an antagonist of adenosine
• The need for sleep, or pressure to sleep is lowest after a good night’s sleep and then starts to build up as we awaken. The need to sleep will rise until we get to sleep.
• Adenosine is a neuromodulator that has an inhibitory (i.e. decreases) effect on neural activity.
• In times of increased brain activity glycogen stored in astrocytes is converted into glucose to fuel neurons.
• When glycogen levels start to fall (energy depletion), adenosine starts to accumulate.
• Caffeine blocks adenosine receptors.
• During SWS, neurons in the brain rest and the astrocytes renew their stock of glycogen.
• If wakefulness is prolonged even more adenosine accumulates.
  Since adenosine inhibits neural activity, it can produce the cognitive and emotional effects seen during sleep deprivation.

Question 24

neurochemical control of arousal- the arousal spectrum

Answer 24

• Instead of only considering one being “awake” or “asleep” we should be thinking about the arousal spectrum.
• There are five key neurotransmitters that can influence where someone lies on the spectrum:
  
  • Acetylcholine (ACh)
  • Norepinephrine (NE)
  • Serotonin (5HT)
  • Histamine (HA)
    Orexin (Hypocretin)

Question 25

neurochemcial control of arousal- acetylcholine (ACh)

Answer 25

• Acetylcholine is released from the cortex and hippocampus.
• It is involved in desynchronised activity in the pons and the basal forebrain.
• ACh antagonists decrease EEG arousal and agonists increase it.
  Important for REM sleep and waking you up - also associated with visual processing in dreams

Question 26

neurochemical control of arousal- noradrenaline

Answer 26

• Norepinephrine, or noradrenaline, is located in the locus coeruleus (LC) of the pons.
• LC is a small nucleus in the dorsal pons that is involved in directing attention.
• Activation of LC neurons increases vigilance.
  Noradrenaline agonists such as amphetamines produce arousal and sleeplessness.

Question 27

neurochemical control of arousal- serotonin (5-HT)

Answer 27

• Serotonin is produced by raphe nuclei (located in the pontine and medullary regions of the reticular formation)
• Stimulation of the raphe nuclei causes movement and arousal.
• Serotonin is involved in the activation of continuous automatic behaviours such as pacing, chewing and grooming.
  When an animal engages in orienting responses the activity of serotonergic neurons decrease.

Question 28

neurochemical control of arousal- histamine (HE)

Answer 28

• Histamine is more commonly known in a way.
• Antihistamines are medicines often used to relieve allergy symptoms but they traditionally have a disruptive side-effect for daily tasks…
• they make you sleepy! → they block histamine signalling
• Histaminergic neurons are located in the tuberomammillary nucleus of the hypothalamus and are involved in maintaining wakefulness.
• Histaminergic neurons ‘regulate’ wakefulness by activating neurons in the cortex that drive arousal and by inhibiting neurons that promote sleep.
• Activity is high during waking and low during sleep.
  Blocking activity of histamine neurons increases sleep.

Question 29

neurochemical control of arousal- orexin (hypocretin)

Answer 29

• After more than 10 years of studying narcoleptic dogs, Lin et al. 1999 isolated the gene that caused narcolepsy → this gene encodes a receptor protein that binds to a neuropeptide called orexin.
• Narcolepsy has been associated to problems with orexin signalling
  
  • degeneration of orexin neurons in humans
  • hereditary absence of orexin receptors in dogs
• Orexin neurons (only 7000) are located in lateral hypothalamus and project to almost all areas of the brain:
  
  • cortex and areas relevant to all of the previous neurotransmitters
  • Orexins have a wakefulness promoting effect
    Active during wakefulness and inactive during sleep

Question 30

neurochemical control of slow wave sleep- the preoptic area

Answer 30

• When we are awake and alert, most of our neurons, especially in the forebrain are active → the level of activity is controlled by the 5 neurotransmitters described earlier
• What controls the activity of the arousal neurons?
  
  • Remember Von Economo insomnia patients?
• They had damage of the anterior hypothalamus
• Nowadays this region is called PREOPTIC AREA:
  It contains neurons whose axons form inhibitory synaptic connections with the brain’s arousal neurons

Question 31

neurochemical control of SW sleep- the ventrolateral preoptic area

Answer 31

• The majority of ‘sleep neurons’ (inhibit arousal neurons) are located in the ventrolateral preoptic area (VLPA).
• When the VLPA neurons become active they suppress the activity of the arousal neurons:
  
  • The VLPA induces slow-wave sleep by secreting GABA to inhibit the brainstem and forebrain arousal systems
  • This suppresses alertness and we fall asleep
• What happens if you lesion the VLPA?
  
  • Total insomnia in rats
  • Animals fall into a coma and die after 3 day
• VLPA activity is initiated by adenosine and neurons in VLPA are inhibited by histamine, noradrenaline and serotonin.

Question 32

where is orexin in this

Answer 32

• Orexin stabilises and tips the system towards the waking state - it can control the flip-flop mechanism
  
  • Stabilising function: During walking you won’t fall asleep because orexin excites neurons of the arousal system
    Orexin holds the arousal centers in the “on” position

Question 33

what controls the activity of orexin neurons

Answer 33

• During the day orexin neurons receive excitatory input from the biological clock that controls circadian rhythms
  
  • Also, from brain areas that monitor the animal’s nutritional state: Orexigenic neurons stimulate appetite
  • Accumulation of adenosine overcomes excitatory input from other areas and sleep happens
    Conclusion: orexigenic neurons are involved in all three factors that control sleep and wakefulness: homeostatic, allostatic and circadian

Question 34

neurochemical control of REM sleep

Answer 34

• Brain metabolism during REM sleep is as high as in wakefulness
• REM sleep is also controlled by a flip-flop mechanism
• The sleep waking flip-flop determines when we wake and when we sleep
• Once we fall asleep the REM flip-flip flop controls the SWS/REM cycles
  Acetylcholine neurons in the pons fire at high rate during REM (similar to wakefulness) and they are responsible for cerebral activation during wakefulness and REM sleep

Question 35

neurochemical control of REM sleep- REM flip flop

Answer 35

• The switch between REM and non-REM (NREM) sleep is mediated by mutually inhibiting REM-on and REM-off neurons in the pons.
• Only one can be present at a certain time, so in which state is this when awake?
• During waking the REM off receives excitatory input from OREXIN, noradrenergic and serotonergic neurons tipping the switch to the off state
• When the sleep/waking flip-flop switches into the sleep phase SWS begins.
  Excitatory activity to REM off decreases, this tips the switch to REM on

Question 36

circadian control of sleep

Answer 36

• Circadian is a term derived from the Latin phrase “circa diem,” meaning “around a day”.
• Circadian rhythms refer to the 24-hour cycles that form part of the human body’s internal, or biological, clock.
• The most well-known circadian rhythm is the sleep-wake cycle.
• Circadian rhythms are kept on schedule by temporal cues (stimuli) in the environment (also known as zeitgebers).
  The most important zeitgeber is the daily cycle of day and light. Could there be other zeitgebers?

Question 37

time- cognitive Zeitgeber

Answer 37

• Clocks, work and travel schedules place demands on the body to remain alert for certain tasks and social events.
  There is a cognitive pressure to stay on schedule.

Question 38

melatonin- a hormonal Zeitgeber

Answer 38

• Melatonin is released in a daily light-sensitive cycle
  
  • Levels of melatonin begin climbing after dark.
  • Melatonin can influence our circadian rhythm (e.g. melatonin-deficient insomnia)
    Melatonin supplements may help individuals reset their circadian rhythm

Question 39

supracharismatic nucleus

Answer 39

• The suprachiasmatic nucleus (SCN) of the hypothalamus is considered to be the circadian clock.
• It receives light inputs from the retina and resets the clock everyday accordingly to the day-night cycle.
• The SCN is most active during the day and least active at night.
• The VLPA is inhibited by the SCN (remember the flip-flop)
  Light-induced activation of SCN prevents the production of melatonin by pineal gland

Question 40

jet lag

Answer 40

• Jet lag occurs when zeitgebers are accelerated (phase advances) during eastbound flights (e.g. going to Thailand) or decelerated (phase delays) during westbound flights (e.g. going to US)
• Results in sleep disturbances, fatigue, mood changes, deficits on tests of physical and cognitive performance.
  Temporary problem treatable with light exposure or melatonin administration.

Question 41

shift work

Answer 41

• In shift work, zeitgebers stay the same but workers are forced to adjust their natural S-W cycles to meet the demands of changing work schedules.
• It can take 1 day for the circadian rhythm to adapt to 1 hour change in light/dark cycle.
  Shift work disorder is related to fatigue, poor performance and poor memory as well as a risk of other health problems (e.g. cardiovascular disease, depression, diabetes).

Question 42

sleep disorders

Answer 42

• Many sleep disorders fall into one of two categories: insomnia and hypersomnia.
  
  • Insomnia includes all disorders of initiating and maintaining sleep.
  • Hypersomnia includes disorders of excessive sleep or sleepiness.
• Another type of sleep disorders includes those related to REM-sleep dysfunction.
  Parasomnias: abnormal behaviours emanating from or associated with sleep

Question 43

insomnia

Answer 43

• Insomnia affects 25% of the population occasionally and 9% regularly.
• Insomnia can be defined in relation to a person’s particular sleep needs.
• Many cases of insomnia are iatrogenic (physician-created) and caused by an increased tolerance and later withdrawal symptoms to sleeping pills (e.g. benzodiazepines).
• Other causes of insomnia can include stress, anxiety, environmental factors (e.g. noise levels, temperature extremes), pain, medications and more.
• Insomnia can also be associated with sleep apnea where the patient stops breathing many times each night and only wake up to breathe again and then drift back to sleep.
• Periodic limb movement disorder is characterized by periodic involuntary movements of the limbs, often involving twitches of the legs during sleep, but patients are unaware
  
  • → this can result in poor sleep and daytime sleepiness
    Restless leg syndrome is characterized by a tension and discomfort in patients’ legs that prevents them from falling asleep (aware).

Question 44

NREM parasomnias

Answer 44

• Confusional arousals:
  
  • Disoriented behaviour during arousal from NREM sleep
  • Last for seconds to minutes
  • Poor recall of events the following day.
• Sleepwalking:
  
  • Up to 17% in children and 4% of adult population
  • Combination of moving with the persistence of impaired consciousness
    Linked with anxiety, fatigue, alcohol, medications and mental disorders

Question 45

REM parasomnias

Answer 45

• REM sleeping behaviour disorder
  
  • Loss of normal atonia: dream enactment behaviour
  • It can often result in injuries
  • More frequent in males >50 years old.
  • Associated to neurodegenerative disorders (Parkinson’s, dementia).
  • Some genetic component.
  • Treated with clonazepam, a benzodiazepine.
• Isolated sleep paralysis (inability to move)
  
  • Paralysis is maintained after waking from REM sleep.
  • It can also occur when falling asleep.
  • Patients are fully aware of what is happening.
  • It can last for seconds to minutes.
  • It is sometimes accompanied by hallucinations.
    It first appears during adolescence but most often in 20s and 30s

Question 46

sleep and cognitive performance

Answer 46

• Sleep is a period where the brain consolidates memories.
• Areas of the brain that are important in memory are active during sleep:
  
  • Hippocampus
  • Neocortex
  • Amygdala
• The quantity and quality of sleep affect a person’s ability to remember.
• Sleep deprivation impairs attention and working (short term) memory, but it also affects as long-term memory and decision-making.
• Hypersomnia (typically results in poor sleep quality) is linked with poor memory.
• Researchers believe that sleep affects learning and memory in two ways:
  
  • Lack of sleep impairs the ability to focus and learn effectively
    Sleep is necessary to consolidate a memory so that it can be recalled in the future

Question 47

how might sleep affect memory?

Answer 47

• Blood flow problems could hinder brain functioning
  Sleep deprived mice have beta amyloid plaques. Beta amyloid deposits are linked to decline in memory and risk of dementia.

Question 48

cerebral blood flow and sleep

Answer 48

• Our brain is critically dependent on continuous and adequate blood supply to function properly.
• When we engage in cognitively demanding tasks our neuronal activity increases and there is an additional demand of nutrients which is provided by increased blood flow.
• This is known as neurovascular coupling or functional hyperemia.
• The brain’s high energy demands are met by a sufficient supply of oxygen and energy substrates from the blood.
• Sleep deprivation can lead to high blood pressure, diabetes and narrowed blood vessels.
• This can in turn decrease blood flow inside the brain.
• If our neurons don’t get the nutrients they need for good cognitive performance through neurovascular coupling, our performance will be impaired.
• To think about…
  
  • If functional magnetic resonance imaging (fMRI) measures are based on
    chemical changes in blood flow as a result of brain activity (e.g. BOLD signal), would fMRI studies be useful in studying the effects of sleep on cognition?

Question 49

impaired sleep and Alzheimers

Answer 49

• Impaired sleep has been associated with Alzheimer’s disease. Studies suggest that sleep plays a role in clearing beta-amyloid out of the brain.
• In a PET study, researchers scanned participants’ brains after normal sleep and a night of sleep deprivation (31 hours without sleep).
• Researchers found that beta-amyloid increased about 5% in the participants’ brains after losing a night of sleep.
  Some of these changes occurred in the thalamus and hippocampus, which are especially vulnerable to damage in the early stages of Alzheimer’s disease.

Question 50

fMRI, hippocampus and memory

Answer 50

• Sleep deprived students asked to view and remember images
• Performed as much as 40% worse on recall two days later
• Activity was significantly decreased in the hippocampus
• Analogous to a lesion on the hippocampus
• Memory impairment rather than concentration
  Memories ‘jammed’ in the hippocampus

Question 51

too much sleep- also an issue

Answer 51

• Sleep quality also important for memory formation (not just quantity; disrupted shorter sleep is often associated with reduced quality and so are changes in sleeping habits/patterns)
• Hypersomnia typically linked with poor sleep quality
• Nurses Health study (Devore et al., 2014)
• 15,385 female nurses reported sleep duration in 1986 (midlife) and 2000 (later life)
• Worse memory performance in those sleeping <5 hours or >9 hours (compared to those who slept 7-8 hours)
  Under-sleepers and over-sleepers were ‘mentally older’

Question 52

poor sleep quality in the elderly

Answer 52

• Poor sleep quality linked to memory loss and brain deterioration in the elderly
• Compared to 20 year olds, 70 year olds demonstrate
  
  • 55% decrease in memory
  • 75% reduction in quality of deep sleep
• Deterioration of frontal lobe linked with impaired slow wave activity
  Memories retained in hippocampus and do not reach neocortex

Question 53

other negative influences on memory

Answer 53

• Cortisol (aka our stress hormone)
  
  • High levels disrupt the transfer of information between hippocampus and neocortex
• Adenosine
  
  • Build up of adenosine has been identified as a link between sleep deprivation and poor memory
• Caffeine is an adenosine receptor antagonist
• Sleep interruption
  
  • Makes new memory formation difficult e.g. think of the ‘mommy brain’
• Sleeping pills
  Inhibit the consolidation of memory

Question 54

learning and REM vs NREM sleep

Answer 54

• Tamaki et al. 2020 study
  
  • In this study they trained participants in a visual learning task
  • Then they had a 90 minute nap in an MRI and used a technique known as Magnetic Resonance Spectroscopy which picks up neurotransmitters.
  • They measured GABA and glutamate in visual areas while they slept and also had EEG
  • Participants were woken up and tested on task again
  • Findings
    ○ → In NREM sleep there is a release of glutamate, which was called an excitatory shift
    
    • In REM sleep there was a release of GABA which was called and inhibitory shift
    • → Individuals with more NREM and excitatory shift, did better, the bigger the shift the bigger the improvement. Participants that had more REM sleep had an inhibitory shift which seemed to be less associated to getting better on the task
• Second part of study
  
  • Same participants learning a different task that interfered with the original task and tested them in the original task
  • The participants that did better were the ones that had some NREM but also the inhibitory REM
  • The complementary processing model
    
    • → During NREM the excitatory shift, or increase in glutamate enhances learning through brain plasticity, the brain forms new connections.
    • → The inhibitory shift (release of GABA) during REM stabilises the newly formed connections
      So you if you wake up before REM sleep even if new connections are formed you may forget more of what you have learned as these connections have not been stabilised

Question 55

napping and dreaming

Answer 55

• Napping can be helpful for improving memory
• Dreaming about a task can boost memory for that task
• Some considerations:
  
  • Limit napping to short bursts
  • Target to natural dips in alertness
  • Long naps may interfere with a normal night’s sleep
• Two groups of participants completed online virtual maze goal reaching destination
• After completing half were allowed to nap, those who napped were quicker.
• In the students that napped they recorded brain activity and asked if they had dreamt.
• Those who dreamed or had EEG evidence of dreaming were the quickest.
• You can’t control dreams but you can nap.
  Good times for napping is after lunch, some Universities are introducing napping pods in exam times.

Question 56

can sleep increase creativity

Answer 56

-Lacaux et al., 2011
- Researchers found that when participants spent at least 15s in Stage 1 sleep (N1), their chance to discover the hidden rule increased (83% versus 30% when they remained awake).
This effect disappeared when subjects reached deeper sleep