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Sleep Flashcards

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The Brain flashcards
1
Q

What is sleep?

A

A behaviour vital for normal functioning, health, well-being and memory

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2
Q

What does it mean that sleep is regulated?

A

if deprived of sleep, we will make up at least part of the sleep when permitted to do so

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3
Q

Where is sleep research conducted?

A

In a sleep lab

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4
Q

What do sleep researchers monitor?

A
  • Electro cephalogram (EEG): brain activity
  • Electromyogram (EMG): muscle activity
  • Electro-oculogram (EOG): eye movements
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5
Q

What are the two basic patterns of brain activity?

A
  • Alpha and beta activity
  • Alpha activity – regular, medium-frequency waves of 8-12 Hz (resting quietly)
  • Beta activity – irregular, mostly low-amplitude waves of 13-30Hz (alert and attentive)
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6
Q

How many times will you cycle through the different stages of sleep in a night?

A

About 4 or 5 times with each cycle lasting about 90 minutes

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7
Q

What happens in stage 1 sleep?

A
  • Become drowsy, enter stage one
  • Theta activity – 3.5 – 7.5 Hz
  • Firing of neurons in the neocortex becomes more synchronised
  • Transition between sleep and wakefulness
  • About 10 minutes
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8
Q

What happens during stage 2 sleep?

A
  • Irregular EEG during this stage
  • Theta activity
  • Sleep spindles – short bursts of waves of 12-14 Hz that occur between 2 and 5 times a minute during sleep
  • K complexes – sudden sharp waveforms usually only found in stage 2
  • K complexes are associated with consolidation of memories and increased numbers of sleep spindles are associated with higher scores on intelligence tests
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9
Q

What happens in stage 3 and 4 slow wave sleep?

A
  • High amplitude delta activity – slower than 3.5 Hz
  • Distinction – stage 3 sees 30-50% delta activity; stage 4 over 50% delta activity
  • Slow wave oscillations < 1 Hz, down state and up state
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10
Q

What happens in REM sleep?

A
  • EEG desynchrony – rapid, irregular waves
  • This is the stage of sleep in which we dream
  • Profound loss of muscle tone – paralysis
  • If woken the person will usually appear attentive and alert
  • Cerebral blood flow and oxygen consumption are accelerated
  • Mechanisms that regulate body temperature stop working
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11
Q

What are the functions of slow-wave sleep?

A
  • Most researchers believe slow-wave sleep allows the brain to rest
  • All mammals sleep, some with only one hemisphere at a time if necessary (dolphins)
  • Slow-wave sleep deprivation affects cognitive abilities, especially sustained attention, but not physical abilities
  • Cerebral metabolic rate and blood flow falls by about 75%
  • This coupled with people’s unresponsiveness and confusion if awakened suggest cerebral cortex ‘shuts down’ during sleep
  • Obviously does give us rest BUT the amount we sleep is not related to the amount of exercise we have done that day
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12
Q

What is the rebound phenomenon?

A

If deprived of REM sleep, you will have more REM sleep in the next sleep period

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13
Q

What is thought to be the function of REM sleep?

A

To help with learning

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14
Q

When does the highest proportion of REM sleep occur?

A

during brain development

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15
Q

What is sleep probably important for?

A

The consolidation of memories

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16
Q

What are the two very broad types of memory?

A

 Declarative (explicit – what you memorise)

 Nondeclarative (implicit – automatic)

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17
Q

What was Mednick, Nakayama & Stickgold’s experiment of implicit memory and sleep?

A

 Participants learned a nondeclarative (implicit) visual discrimination task at 9am
 Some participants took a 90min nap during the day
 Used EEG to see which participants engaged in REM sleep and which did not
 Participants performed the task again at 7pm that night
 They found that those that did not have a nap performed worse at 7pm that 9am
 Those that had a nap but didn’t get any REM sleep performed at the same level
 Those who had a nap and got REM sleep performed better
 Suggest that REM sleep important for implicit memories

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18
Q

What was Tucker’s nondeclarative vs declarative memory experiment with sleep?

A

 Trained participants on a nondeclarative and declarative task
 Some participants had a one hour nap
 But were awakened before they engaged in REM sleep
 So those who napped, engaged in slow-wave sleep only
 Found that compared to those who had no sleep those who had a nap performed better on the declarative learning task but not on the nondeclarative task

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19
Q

It terms of memories what does REM sleep and slow wave sleep facilitate?

A

 REM sleep facilitates consolidation of nondeclarative memories
 Slow wave sleep facilitates consolidation of declarative memories

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20
Q

What do studies by Peigneaux and Wamsley show in relation to slow wave sleep and navigation?

A

 Both studies confirmed a role of slow-wave sleep in learning our way around
 We appear to rehearse the information during slow-wave sleep and consolidate learning

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21
Q

What are the different neurotransmitters that play a role in arousal?

A
  • acetylcholine
  • norepinephrine
  • serotonin
  • histamine
  • orexin
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22
Q

Where is acetylcholine found and how is it related to arousal?

A
  • Levels high in the hippocampus and neocortex (Marrosu et al. 1995)
  • Activating AcH neurons in the basal forebrain causes wakefulness (Cape and Jones, 2000)
  • High levels of acetylcholine activation during both waking and REM sleep
  • Acetylcholine production low during slow wave sleep
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23
Q

How is noradrenaline related to arousal?

A
  • Activity of noradrenergic locus coeruleus neurons increases vigilance
  • Increases during wakefulness
  • Moment-to-moment activity of noradrenergic LC neurons related to performance on task requiring vigilance
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24
Q

How is serotonin related to arousal and sleep?

A
  • Involved in numerous processes
  • Stimulation of raphe nuclei (where most of the serotonergic neurons are found) causes locomotion and cortical arousal
  • Serotonergic neurons are most active during waking, steadily decline during sleep to almost zero activity in REM sleep
  • Temporarily becomes very active after REM sleep
25
Q

Where are histaminergic neurons and how is histamine related to sleep and arousal?

A
  • Histaminergic neurons are located in the hypothalamus
  • Drugs that prevent the synthesis of histamine of block histamine receptors decrease waking and increase sleep (Lin et al., 1998)
  • Activity of histaminergic neurons is high during waking and low during slow wave sleep and REM sleep
26
Q

What is another name for Orexin?

A

hypocretin

27
Q

Where are cell bodies that secrete Orexin located?

A

In the hypothalamus

28
Q

How is Orexin related to arousal?

A
  • Excitatory effect in the cerebral cortex and all other regions involved in arousal and wakefulness
  • Activating neurons in the lateral hypothalamus of mice awakens the animals from REM and non-REM sleep
  • Orexinergic neurons in rats fire fastest in active waking, particularly when exploring and fire less frequently during quiet waking and sleep
29
Q

What 3 factors is sleep controlled by?

A

homeostatic, allostatic, and circadian

30
Q

How does the homeostatic factor work in controlling sleeo?

A
  • adenosine builds up in the brain when we are awake
  • Adenosine is a neuromodulator released by neurons relating in high levels of activity
  • when we sleep it is probably broken down
31
Q

What is allostatic control mediated by and what does it allow us to do?

A
  • Allostatic controlled is mediated by hormonal and neural responses to stressful situations
     Allows us to override homeostatic factors if we need to stay awake
32
Q

What is Circadian control?

A

Our biological rhythm

33
Q

What inhibits the arousal system when we need to sleep?

A

Group of GABAnergic neurons in the ventrolateral preoptic area (vIPOA) become active and supress activity of arousal neurons

34
Q

What can lead to insomnia?

A

Lesions of GABA

35
Q

What is the sleep-waking flip-flop?

A

 The flip-flop is on when the sleep-promoting neurons in the VIPOA are inhibited and the arousal neurons are active
 The flip-flop is off when the sleep-promoting neurons in the vIPOA are activated and the arousal neurons are inhibited

36
Q

What helps to stabilise the sleep-waking flip-flop?

A

Orexinergic neurons

37
Q

what activates the orexinergic neurons?

A

motivation to remain awake or events that disturb the sleep

38
Q

What do the brain stem and forebrain arousal systems usually activate when the sleep-waking flip-flop is on?

A

usually activate ACh, NE, 5HT and histamine

39
Q

What factors control the activity of the orexinergic neurons?

A

 Biological clock
 Hunger related signals activate them
 Satiety related signals inhibit them
 Orexinergic neurons receiving inhibitory input from the vIPOA because of a build-up of adenosine

40
Q

Where are REM-ON and REM-OFF neurons located?

A
  • REM-ON neurons are located in the pons

- REM-OFF neurons are located in the midbrain

41
Q

What happens with the REM flip-flop?

A
  • During waking, the REM-OFF region receives excitatory input from the orexinergic neurons of the lateral hypothalamus, and this activation tips the REM flip-flop into the OFF state
  • When the sleep/waking flip-flop switches into the sleep phase, slow wave sleep begins
  • The activity of the excitatory orexinergic, noradrenergic and serotonergic inputs to the REM-OFF region begins to decrease. As a consequence the excitatory input to the REM-OFF region is removed
  • The REM flip-flop tips to the ON state and REM sleep begins
42
Q

What can emotional stimuli do regarding the REM flip-flop?

A
  • Emotional stimuli activates the Amygdala which leads to the REM-ON state
43
Q

What happens when the REM flip-flop tips to the ON state in terms of the spinal cord?

A

When the REM flip-flop tips to the ON state, motor neurons in the spinal cord become inhibited, and cannot respond to the signals arising from the motor cortex in the course of a dream

44
Q

When may a person act out their dreams?

A

If their ‘paralysis neurons’ are damaged

45
Q

What is insomnia, how many people does it effect and when would you be diagnosed with it?

A
  • Difficulty getting to sleep, staying asleep, or having non-restorative sleep
  • Together with associated impairment of daytime functioning
  • Defined in relation to a person’s particular need for sleep
  • Chronic insomnia effects approximately 9% of the population while up to 1/3 report at least one nocturnal symptom
  • Symptoms need to be present for 4 weeks to get diagnosis
46
Q

What are causes of insomnia?

A

 Age: more common in older people
 Environmental factors: electronic devices, noise, light (white noise or other repetitive noise is beneficial)
 Physiology (heightened activity in the reticular activating system – involved with arousal)
 Circadian rhythms: changes, e.g. through time zone, shift-work patterns
 Medical conditions and medications: heart and respiratory conditions, some antidepressants and epilepsy medications

47
Q

What are treatments for insomnia?

A

 Typically treated with drugs but can potentially also be treated with mindfulness and CBT
 Chronic sleep deprivation can lead to serious health problems, e.g. obesity, diabetes and CVD

48
Q

What is sleep apnea?

A
  • Form of insomnia – the inability to sleep and breathe at the same time
  • Build of carbon dioxide
  • Carbon dioxide in the blood stimulates chemoreceptors, person wakes up gasping for air
  • Disrupts sleep affecting daytime functioning
49
Q

If sleep apnea is caused by obstruction how can it be treated?

A

If caused by obstruction can be corrected surgically or relieved by pressurised air that keeps the airway open

50
Q

What are some symptoms of narcolepsy?

A

 Sleep attack – overwhelming urge to sleep
 Cataplexy – muscular paralysis of REM sleep while awake:
- Varying degrees of muscle weakness
- Can become completely paralysed while conscious
- Generally occurs when the person feels strong emotions or by sudden physical effort
 Sleep paralysis: REM muscular paralysis just before the onset of sleep or upon waking
 Hypnagogic hallucinations
- Dreaming while awake and paralysed
- Very realistic and terrifying
- Some deficiency in REM flip-flop

51
Q

What are the causes of Narcolepsy?

A

 Hereditary element
 Environmental factors play a role but are unknown
 Orexinergic neurons are attacked by the immune system, usually in adolescence (REM flip-flop becomes unstable)
 Emotional stimuli activating amygdala

52
Q

What is the treatment for narcolepsy?

A

 Sleep attacks can be diminished with stimulants such as methylphenidate (Ritalin)
 REM sleep phenomenon (cataplexy, sleep paralysis and hypagogic hallucinations) traditionally treated with antidepressant drugs
 Most common current treatments are modafinil and/or sodium oxybate, both stimulant drugs

53
Q

What is REM sleep behaviour disorder and how is it usually treated?

A
  • Failure to exhibit paralysis during REM sleep
  • Acting out dreams
  • Neurodegenerative disorder with a genetic component
  • Associated with other neurodegenerative conditions such as Parkinson’s disease
  • Usually treated with clonazepam, a benzodiazepine tranquilizer
54
Q

What are some slow-wave sleep problems?

A
  • sleepwalking
  • night terrors
  • bedwetting
55
Q

What is sleepwalking (somnambulism)?

A

 Not acting out a dream but the person can engage in complex behaviours
 More common in children (2x as common)
 Genetic component
 Disorder of arousal

56
Q

What are night terrors and what causes them?

A

 Anguished screams, trembling, a rapid pulse, and usually no memory of what caused the terror
 Hereditary element

57
Q

Give features of bedwetting?

A

 Genetic link
 Can be characterised as heavy sleepers
 About 10% of 7 year olds

58
Q

What is Fatal Familial insomnia and what symptoms does it cause?

A
  • Neurodegenerative condition
  • Prion disease (build up of abnormal prion proteins that are resistant to being broken down by enzymes)
  • Damage to the thalamus
  • Initially presents with insomnia and very vivid dreams when the person finally manages to sleep
  • Psychiatric complications – panic attacks, cognitive deficits, paranoia and phobias
  • As the disease progresses it affects the autonomic nervous system (elevated blood pressure) and coordination (ataxia)
59
Q

What does an EEG show with fatal familial insomnia and what does it result in?

A
  • Disappearance of slow-wave sleep and only brief periods of REM sleep
  • Ultimately inability to voluntarily move or speak (akinetic mutism), coma and death

Brain and Behaviour (11 decks)

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