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sleep Flashcards

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1
Q

what is sleep?

A

sleep is a regulated behaviour

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2
Q

what is sleep vital for?

A

normal functioning
health
well being
memory

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3
Q

where is sleep research conducted?

A

in a sleep laboratory

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4
Q

what do researchers interested in sleep measure?

A

EEG
EMG
EOG
heart rate, respiration, skin conduction

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5
Q

EEG

A

electroencephalogram- brain activity

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6
Q

EMG

A

electromyogram - muscleactivity

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7
Q

EOG

A

electro-oculogram

eye movements

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8
Q

what are teh two basic patterns of brain activity during wakefulness?

A

beta activity and alpha activity

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9
Q

beta activity frequency range

A

13-30 Hz

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10
Q

beta activity

A

alert, attentive, active thinking

many different neural circuits in teh brain are actively processing information

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11
Q

alpha activity frequency

A

8-12 Hz

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12
Q

alpha activity

A

resting quietly
not aroused or excited
not engaged in strenuous mental activity
usually occurs when eyes are closed

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13
Q

theta activity

A

3.3-7.5 Hz
stages 1 and 2
REM

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14
Q

delta activity

A

<3.5 Hz

stages 3 and 4

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15
Q

what happens as sleep deepens

A

frequency of brain activity decreases

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16
Q

stages of sleep in order

A 
wakefulness 
stage 1
stage 2
REM 
stage 3 
stage 4
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17
Q

stage 1 sleep

A

transition between sleep and wakefulness (drowsy)

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18
Q

how long does stage 1 sleep last

A

approx 10 mins

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19
Q

EEG during stage 1 sleep

A

firing of neurons in the neocortex become more synchronised

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20
Q

stage 2 sleep

A

if people awakened, they may report that they have not been asleep

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21
Q

how long does stage 2 sleep last?

A

approximately 15 minutes

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22
Q

EEG stage 2

A

irregular
sleep spindles
k complexes

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23
Q

sleep spindles

A

short bursts of waves 12-14 Hz

occur between 2 and 5 times a minute during sleep stages 1-4

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24
Q

what are increased numbers of sleep spindles associated with?

A

higher scores on intelligence test

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25
Q

k complexes

A

sudden sharp waveforms usually only found in stage 2
associated with a consolidation of memories
forerunner of deltawaves

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26
Q

stages 3 and 4 are called?

A

slow wave sleep

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27
Q

stage 3 & 4

A

only loud noises will wake people up

when awakened, the person acts groggy and confused

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28
Q

distinction between stage 3 and stage 4

A

stage 3: 20-50% delta activity

stage 4: over 50% delta activity

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29
Q

slow wave oscillations, frequency and types?

A 
most important feature of slow wave sleep 
<1Hz
down state (off) 
up state (on)
moderate muscle tonus 
slow or absent eye movements
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30
Q

down state (off)

A

neurons in the cortex are absolutely silent - neurons are able to rest

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31
Q

up state (on)

A

period of excitation during which these neurons briefly fire at a high rate

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32
Q

REM sleep EEG

A

desynchrony

rapid, irregular

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33
Q

physiological changes associated with REM

A

rapid eye movements

profound loss of muscle tone- paralysis

mechanisms that regulate body temperature stop working

brain is active: cerebral blood flow and consumption are accelerated

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34
Q

REM sleep

A

we dream
people react to meaningful stimuli (e.g. name)
if woken the person will usually appear attentive and alert

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35
Q

when do humans sleep with only one hemisphere of their brain?

A

first night effect

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36
Q

first night effect (FNE)

A

troubled sleep in a novel environment

one hemisphere being more vigilant than the other to monitor unfamiliar surroundings during sleep

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37
Q

functions of slow wave sleep

A

allows the brain to rest

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38
Q

how does slow wave sleep allow the brain to rest?

A

cerebral metabolic rate and blood flow falls by about 75%

suggested that the cerebral cortex shuts down during sleep

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39
Q

why is it suggested the cerebral cortex shuts down in stage 3&4

A

reduced metabolic rate and blood floe
peoples unresponsiveness
confusion if awakened

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40
Q

what does slow wave sleep deprivation effect?

A

cognitive abilities, especially sustained attention, but not physical abilities

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41
Q

is sleep related to exercise?

A

the amount we exercise in a day does not affect the amount we sleep

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42
Q

rebound phenomenon:

A

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

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43
Q

is it possible to function with no REM sleep?

A

yes, with no side effect s

this is shown by people on antidepressants or with brain damage that reduces or eliminates REM sleep

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44
Q

possible functions of REM sleep

A

promotes learning

brain development

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45
Q

REM sleep and brain development

A

facilitates massive changes in the brain

highest proportion of REM sleep occurs during brain development

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46
Q

criticism against link between REM and brain development

A

adults still have REM sleep

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47
Q

two broad types of memory

A

declarative and non declarative (explicit and implicit)

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48
Q

Mednick, Nakayama, & Stickgold (2003) method

A

Participants learned a nondeclarative
(implicit) visual texture discrimination
task at 9am

Participants groups:
• Nap (90 mins) - Used EEG to see which
participants engaged in REM sleep and
which participants did not.
• No nap

Participants performed the task again
at 7pm that night

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49
Q

Mednick, Nakayama, & Stickgold (2003) results

A

Only after a 90-minute nap that included
both slow-wave sleep and REM sleep did the
subjects’ performance improve.

50
Q

Mednick, Nakayama, & Stickgold (2003) interpretation of results

A

REM sleep is important for implicit (non declarative) learning

51
Q

Tucker et al. (2006) method

A

trained participants on a non declarative and declarative task

60 participants
-60 min nap- awakened before they engaged in REM sleep

6 hours later participants performance was tested

52
Q

tucker et al (2006) results

A

slow wave seep improved performance on declarative task compared to no sleep participants
participants engaged in slow wave sleep did not show more engagement than no sleep participants on non declarative task

53
Q

tucker et al (2006) interpretation of results

A

slow wave sleep affects declarative performance

54
Q

sleep an dlearning

A

REM sleep facilitates consolidation of non declarative memories

slow wave sleep facilitates consolidation of declarative memories

55
Q

role of slow wave sleep in navigation

A

participants learned their way around a virtual town

this is a declarative form of learning

56
Q

what do we do with information during slow wave sleep?

A

rehearse the information and consolidate learning

activity of the hippocampus during learning and slow wave sound sleep

57
Q

5 neurotransmitters that play a role in arousal (alertness and wakefulness)

A 
acetylcholine 
norepinephrine 
serotonin 
histamine 
orexin
58
Q

when do we have high levels of ACh

A

when we awake (QW, AW) or in REM sleep

59
Q

when do we have low levels of acetylcholine?

A

during slow wave sleep

60
Q

what are the hippocampus and neocortex related to?

A

alertness

61
Q

what does activating ACh neurones in the basal forebrain cause?

A

wakefulness

62
Q

what does activity of the noradrenergic locus coeruleus neurons increase?

A

vigilance

63
Q

when does activity of noradrenergic locus coeruleus neurons increas ?

A

during wakefulness

64
Q

when is activity of noradrenergic locus

coeruleus neurons low?

A

during slow wave sleep

65
Q

when is activity of noradrenergic locus

coeruleus neurons almost 0?

A

during REM sleep

66
Q

what is moment to moment activity of noradrenergic LC neurons related to?

A

performance on tasks requiring vigilance

67
Q

where are most serotonergic neurons found?

A

in the raphe nuclei

68
Q

what does stimulation of the raphe nuclei cause?

A

cortical arousal

69
Q

what happens if you block teh synthesis of serotonin?

A

arousal is reduced

70
Q

activity of serotonergic neurons during stages of sleep

A

most active during waking
steadily decline to almost 0 activity by REM sleep
temporarily become very active after REM sleep

71
Q

where are histaminergic neurons located?

A

in the hypothalamus

72
Q

when is activity of histaminergic neurons high?

A

during waking

73
Q

when is activity of histaminergic neurons low?

A

during slow wave and REM sleep

74
Q

what is teh effect of drugs that prevent the synthesis of histamine or block histamine receptors?

A

decrease waking

increase sleep

75
Q

where are cell bodies that secrete orexin?

A

in the lateral hypothalamus

76
Q

what is the effect of orexin?

A

it has an excitatory effect in the cerebral cortex and all other regions involved in arousal and wakefulness

77
Q

activation of orexinergic neurons

A

awakens mice form REM and non REM sleep

78
Q

when do orexinergic neurons fire fastest?

A

in active walking

particularly when exploring

79
Q

when do orexinergic neurons fire less frequently?

A

during quiet walking and sleep

80
Q

what 3 factors is sleep controlled by?

A

homeostatic
allostatic
circadian

81
Q

primary homeostatic factor

A

presence or absence of adenosine

neuromodulator
released by active neurons, builds up while we are awake
destroyed by slow wave sleep

82
Q

what is allosteric control mediated by?

A

hormonal and neural responses to stressful situations

83
Q

what is necessary for sleep?

A

inhibition of the arousal system

84
Q

what are sleep promoting neurons?

A

group of GABAnergic neurons (preoptic neuron ) in the ventrolateral preoptic area of the hypothalamus

85
Q

what is the action of sleep promoting neurons?

A

to supress activity of arousal neurons

86
Q

flip flop on: we are awake

A

when sleep promoting neurons in the vIPOA are inhibited and the arousal neurons are active

87
Q

flip flop off: we are asleep

A

when teh sleep-promoting neurons in the vIPOA are activates and the arousal neurons are inhibited

88
Q

what to neurons involved in sleep cannot be active at the same time?

A

sleep promoting neurons and arousal neurons

89
Q

vIPOA

A

ventrolateral preoptic area

90
Q

what do orexinergic neurons help stabalise?

A

the sleep/waking flip/flop

91
Q

what activates orexinergic neurons

A

motivation to remain awake or events that disturb sleep

92
Q

what factors control the activity of orexinergic signals?

A

inhibitory:
input to vlPOA because of build up of adenosine
satiety related signals

excitatory: hunger related signals
other: biological clock

93
Q

where are REM on neurons located?

A

in the pons

94
Q

where are REM off neurons located?

A

in the midbrain- VlPAG

95
Q

waking: REM off

A

REM off region receives excitatory input from orexinergic neurons and this activation tips teh REM flip-flop into the off state

96
Q

REM sleep- REM on

A

orexinergic input to REM OFF starts to decrease

The REM flip-flop tips to the on state, REM sleep begins

97
Q

Paralysis during REM

A

specific neurons control the muscular paralysis during REM sleep

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

98
Q

what are the effects of damage to the ‘paralysis neurons’

A

no inhibition of motor neurons

person acts out their dream

99
Q

DSM-V criteria for insomnia

A

difficulty getting to sleep, staying asleep or having non-restorative sleep

together with associated impairment of daytime functioning

defined in relation to a particular persons relationship w sleep

100
Q

how many people are affected by insomnia?

A

9% of the population

1/3 report at least one nocturnal symptom

101
Q

causes of insomnia

A

age: more common when older
stress
environmental factors
-electronic devices, noise and light
detrimental
-white noise or other repetitive noise
beneficial
physiology: heightened activity in the reticular activating system
changes in circadian rhythms
medical conditions

102
Q

treatment of insomnia

A

typically treated with drugs

can be treated with mindfulness

chronic sleep deprivation can lead to serious health problems
-obesity, diabetes, cardiovascular disease

103
Q

sleep apnea

A

form of insomnia
inability to sleep and breath at the same time

leads to a build up of carbon dioxide in the blood that stimulates chemoreceptors, causing person to wake up gasping for air

104
Q

effect of sleep apnea

A

disrupts sleep affecting daytime functioning

105
Q

can sleep apnea be corrected?

A

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

106
Q

narcolepsy symptoms

A

sleep attack
cataplexy
sleep paralysis
hypnagogic hallucinations

107
Q

sleep attack

A

overwhelming urge to sleep

108
Q

cataplexy

A

muscular paralysis of REM sleep while awake

  • varying degrees of muscle weakness
  • can become completely paralysed while conscious
  • occurs when a person feels strong emotions or by sudden physical effort
109
Q

sleep paralysis

A

REM muscular paralysis just before the onset of sleep or upon waking up

110
Q

hypnagogic hallucinations

A

dreaming while awake and paralysed

can be realistic and terrifying

111
Q

causes of narcolepsy

A

hereditary element

environmental factors play a role but are unknown

orexinergic neurons are attacked by the immune system, normally in childhood

112
Q

treatments of narcolepsy

A

sleep attacks can be diminished with stimulants such as: methylphenidate

REM sleep phenomenon typically treated with antidepressant drugs

most common current treatments: modafanil and/or sodium oxybate
both stimulant drugs

113
Q

REM sleep behaviour disorder

A

failure to exhibit paralysis during REM sleep

acting out dreams

neurodegenerative disorder with genetic component (associated with neurodegenerative conditions such as Parkinson’s)

114
Q

how is REM sleep behaviour disorder usually treated?

A

with clonazepam , a benzodiazepine tranquiliser

115
Q

slow wave sleep problems

A 
sleep walking (somnambulism) 
night terrors (pavor nocturnus) 
bedwetting (nocturnal enuresis)

most frequently occur in children and all have hereditary elements

116
Q

somnambulism

A

disorder of arousal

person can engage in complex behaviours

117
Q

pavor nocturnus

A

anguished screams, trembling, a rapid pulse, usually no memory for what caused the terror

118
Q

bedwetting

A

10% of 7 year olds

119
Q

fatal familial insomnia

A

neurodegenerative condition caused by damage to the thalamus
prion disease

120
Q

symptoms of fatal familial insomnia

A

Initially presents with insomnia and very vivid dreams when the person finally
manages to sleep - EEG shows disturbances and reductions in sleep spindles and K
complexes

Disappearance of slow-wave sleep and only brief periods of REM sleep

deficits in attention and memory, followed by a dreamlike, confused state

As the disease progresses it affects the autonomic nervous system (e.g. elevated
blood pressure) and coordination (ataxia)

Psychiatric complications – panic attacks, cognitive deficits, paranoia and phobias

Ultimately inability to voluntarily move or speak (akinetic mutism), coma, and death.

brain and behaviour (12 decks)

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