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Sleep 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
Where are histaminergic neurons and how is histamine related to sleep and arousal?
- 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
What is another name for Orexin?
hypocretin
27
Where are cell bodies that secrete Orexin located?
In the hypothalamus
28
How is Orexin related to arousal?
- 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
What 3 factors is sleep controlled by?
homeostatic, allostatic, and circadian
30
How does the homeostatic factor work in controlling sleeo?
- 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
What is allostatic control mediated by and what does it allow us to do?
- 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
What is Circadian control?
Our biological rhythm
33
What inhibits the arousal system when we need to sleep?
Group of GABAnergic neurons in the ventrolateral preoptic area (vIPOA) become active and supress activity of arousal neurons
34
What can lead to insomnia?
Lesions of GABA
35
What is the sleep-waking flip-flop?
 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
What helps to stabilise the sleep-waking flip-flop?
Orexinergic neurons
37
what activates the orexinergic neurons?
motivation to remain awake or events that disturb the sleep
38
What do the brain stem and forebrain arousal systems usually activate when the sleep-waking flip-flop is on?
usually activate ACh, NE, 5HT and histamine
39
What factors control the activity of the orexinergic neurons?
 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
Where are REM-ON and REM-OFF neurons located?
- REM-ON neurons are located in the pons | - REM-OFF neurons are located in the midbrain
41
What happens with the REM flip-flop?
- 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
What can emotional stimuli do regarding the REM flip-flop?
- Emotional stimuli activates the Amygdala which leads to the REM-ON state
43
What happens when the REM flip-flop tips to the ON state in terms of the spinal cord?
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
When may a person act out their dreams?
If their 'paralysis neurons' are damaged
45
What is insomnia, how many people does it effect and when would you be diagnosed with it?
- 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
What are causes of insomnia?
 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
What are treatments for insomnia?
 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
What is sleep apnea?
- 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
If sleep apnea is caused by obstruction how can it be treated?
If caused by obstruction can be corrected surgically or relieved by pressurised air that keeps the airway open
50
What are some symptoms of narcolepsy?
 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
What are the causes of Narcolepsy?
 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
What is the treatment for narcolepsy?
 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
What is REM sleep behaviour disorder and how is it usually treated?
- 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
What are some slow-wave sleep problems?
- sleepwalking - night terrors - bedwetting
55
What is sleepwalking (somnambulism)?
 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
What are night terrors and what causes them?
 Anguished screams, trembling, a rapid pulse, and usually no memory of what caused the terror  Hereditary element
57
Give features of bedwetting?
 Genetic link  Can be characterised as heavy sleepers  About 10% of 7 year olds
58
What is Fatal Familial insomnia and what symptoms does it cause?
- 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
What does an EEG show with fatal familial insomnia and what does it result in?
- Disappearance of slow-wave sleep and only brief periods of REM sleep - Ultimately inability to voluntarily move or speak (akinetic mutism), coma and death

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