sleep Flashcards
what is sleep?
sleep is a regulated behaviour
what is sleep vital for?
normal functioning
health
well being
memory
where is sleep research conducted?
in a sleep laboratory
what do researchers interested in sleep measure?
EEG
EMG
EOG
heart rate, respiration, skin conduction
EEG
electroencephalogram- brain activity
EMG
electromyogram - muscleactivity
EOG
electro-oculogram
eye movements
what are teh two basic patterns of brain activity during wakefulness?
beta activity and alpha activity
beta activity frequency range
13-30 Hz
beta activity
alert, attentive, active thinking
many different neural circuits in teh brain are actively processing information
alpha activity frequency
8-12 Hz
alpha activity
resting quietly
not aroused or excited
not engaged in strenuous mental activity
usually occurs when eyes are closed
theta activity
3.3-7.5 Hz
stages 1 and 2
REM
delta activity
<3.5 Hz
stages 3 and 4
what happens as sleep deepens
frequency of brain activity decreases
stages of sleep in order
wakefulness stage 1 stage 2 REM stage 3 stage 4
stage 1 sleep
transition between sleep and wakefulness (drowsy)
how long does stage 1 sleep last
approx 10 mins
EEG during stage 1 sleep
firing of neurons in the neocortex become more synchronised
stage 2 sleep
if people awakened, they may report that they have not been asleep
how long does stage 2 sleep last?
approximately 15 minutes
EEG stage 2
irregular
sleep spindles
k complexes
sleep spindles
short bursts of waves 12-14 Hz
occur between 2 and 5 times a minute during sleep stages 1-4
what are increased numbers of sleep spindles associated with?
higher scores on intelligence test
k complexes
sudden sharp waveforms usually only found in stage 2
associated with a consolidation of memories
forerunner of deltawaves
stages 3 and 4 are called?
slow wave sleep
stage 3 & 4
only loud noises will wake people up
when awakened, the person acts groggy and confused
distinction between stage 3 and stage 4
stage 3: 20-50% delta activity
stage 4: over 50% delta activity
slow wave oscillations, frequency and types?
most important feature of slow wave sleep <1Hz down state (off) up state (on) moderate muscle tonus slow or absent eye movements
down state (off)
neurons in the cortex are absolutely silent - neurons are able to rest
up state (on)
period of excitation during which these neurons briefly fire at a high rate
REM sleep EEG
desynchrony
rapid, irregular
physiological changes associated with REM
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
REM sleep
we dream
people react to meaningful stimuli (e.g. name)
if woken the person will usually appear attentive and alert
when do humans sleep with only one hemisphere of their brain?
first night effect
first night effect (FNE)
troubled sleep in a novel environment
one hemisphere being more vigilant than the other to monitor unfamiliar surroundings during sleep
functions of slow wave sleep
allows the brain to rest
how does slow wave sleep allow the brain to rest?
cerebral metabolic rate and blood flow falls by about 75%
suggested that the cerebral cortex shuts down during sleep
why is it suggested the cerebral cortex shuts down in stage 3&4
reduced metabolic rate and blood floe
peoples unresponsiveness
confusion if awakened
what does slow wave sleep deprivation effect?
cognitive abilities, especially sustained attention, but not physical abilities
is sleep related to exercise?
the amount we exercise in a day does not affect the amount we sleep
rebound phenomenon:
if deprived of REM sleep you will have more REM sleep in the next period
is it possible to function with no REM sleep?
yes, with no side effect s
this is shown by people on antidepressants or with brain damage that reduces or eliminates REM sleep
possible functions of REM sleep
promotes learning
brain development
REM sleep and brain development
facilitates massive changes in the brain
highest proportion of REM sleep occurs during brain development
criticism against link between REM and brain development
adults still have REM sleep
two broad types of memory
declarative and non declarative (explicit and implicit)
Mednick, Nakayama, & Stickgold (2003) method
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
Mednick, Nakayama, & Stickgold (2003) results
Only after a 90-minute nap that included
both slow-wave sleep and REM sleep did the
subjects’ performance improve.
Mednick, Nakayama, & Stickgold (2003) interpretation of results
REM sleep is important for implicit (non declarative) learning
Tucker et al. (2006) method
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
tucker et al (2006) results
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
tucker et al (2006) interpretation of results
slow wave sleep affects declarative performance
sleep an dlearning
REM sleep facilitates consolidation of non declarative memories
slow wave sleep facilitates consolidation of declarative memories
role of slow wave sleep in navigation
participants learned their way around a virtual town
this is a declarative form of learning
what do we do with information during slow wave sleep?
rehearse the information and consolidate learning
activity of the hippocampus during learning and slow wave sound sleep
5 neurotransmitters that play a role in arousal (alertness and wakefulness)
acetylcholine norepinephrine serotonin histamine orexin
when do we have high levels of ACh
when we awake (QW, AW) or in REM sleep
when do we have low levels of acetylcholine?
during slow wave sleep
what are the hippocampus and neocortex related to?
alertness
what does activating ACh neurones in the basal forebrain cause?
wakefulness
what does activity of the noradrenergic locus coeruleus neurons increase?
vigilance
when does activity of noradrenergic locus coeruleus neurons increas ?
during wakefulness
when is activity of noradrenergic locus
coeruleus neurons low?
during slow wave sleep
when is activity of noradrenergic locus
coeruleus neurons almost 0?
during REM sleep
what is moment to moment activity of noradrenergic LC neurons related to?
performance on tasks requiring vigilance
where are most serotonergic neurons found?
in the raphe nuclei
what does stimulation of the raphe nuclei cause?
cortical arousal
what happens if you block teh synthesis of serotonin?
arousal is reduced
activity of serotonergic neurons during stages of sleep
most active during waking
steadily decline to almost 0 activity by REM sleep
temporarily become very active after REM sleep
where are histaminergic neurons located?
in the hypothalamus
when is activity of histaminergic neurons high?
during waking
when is activity of histaminergic neurons low?
during slow wave and REM sleep
what is teh effect of drugs that prevent the synthesis of histamine or block histamine receptors?
decrease waking
increase sleep
where are cell bodies that secrete orexin?
in the lateral hypothalamus
what is the effect of orexin?
it has an excitatory effect in the cerebral cortex and all other regions involved in arousal and wakefulness
activation of orexinergic neurons
awakens mice form REM and non REM sleep
when do orexinergic neurons fire fastest?
in active walking
particularly when exploring
when do orexinergic neurons fire less frequently?
during quiet walking and sleep
what 3 factors is sleep controlled by?
homeostatic
allostatic
circadian
primary homeostatic factor
presence or absence of adenosine
neuromodulator
released by active neurons, builds up while we are awake
destroyed by slow wave sleep
what is allosteric control mediated by?
hormonal and neural responses to stressful situations
what is necessary for sleep?
inhibition of the arousal system
what are sleep promoting neurons?
group of GABAnergic neurons (preoptic neuron ) in the ventrolateral preoptic area of the hypothalamus
what is the action of sleep promoting neurons?
to supress activity of arousal neurons
flip flop on: we are awake
when sleep promoting neurons in the vIPOA are inhibited and the arousal neurons are active
flip flop off: we are asleep
when teh sleep-promoting neurons in the vIPOA are activates and the arousal neurons are inhibited
what to neurons involved in sleep cannot be active at the same time?
sleep promoting neurons and arousal neurons
vIPOA
ventrolateral preoptic area
what do orexinergic neurons help stabalise?
the sleep/waking flip/flop
what activates orexinergic neurons
motivation to remain awake or events that disturb sleep
what factors control the activity of orexinergic signals?
inhibitory:
input to vlPOA because of build up of adenosine
satiety related signals
excitatory: hunger related signals
other: biological clock
where are REM on neurons located?
in the pons
where are REM off neurons located?
in the midbrain- VlPAG
waking: REM off
REM off region receives excitatory input from orexinergic neurons and this activation tips teh REM flip-flop into the off state
REM sleep- REM on
orexinergic input to REM OFF starts to decrease
The REM flip-flop tips to the on state, REM sleep begins
Paralysis during REM
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
what are the effects of damage to the ‘paralysis neurons’
no inhibition of motor neurons
person acts out their dream
DSM-V criteria for insomnia
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
how many people are affected by insomnia?
9% of the population
1/3 report at least one nocturnal symptom
causes of insomnia
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
treatment of insomnia
typically treated with drugs
can be treated with mindfulness
chronic sleep deprivation can lead to serious health problems
-obesity, diabetes, cardiovascular disease
sleep apnea
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
effect of sleep apnea
disrupts sleep affecting daytime functioning
can sleep apnea be corrected?
if caused by obstruction can be corrected surgically or relieved by pressurised air that keeps the airway open
narcolepsy symptoms
sleep attack
cataplexy
sleep paralysis
hypnagogic hallucinations
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
- occurs when a person feels strong emotions or by sudden physical effort
sleep paralysis
REM muscular paralysis just before the onset of sleep or upon waking up
hypnagogic hallucinations
dreaming while awake and paralysed
can be realistic and terrifying
causes of narcolepsy
hereditary element
environmental factors play a role but are unknown
orexinergic neurons are attacked by the immune system, normally in childhood
treatments of narcolepsy
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
REM sleep behaviour disorder
failure to exhibit paralysis during REM sleep
acting out dreams
neurodegenerative disorder with genetic component (associated with neurodegenerative conditions such as Parkinson’s)
how is REM sleep behaviour disorder usually treated?
with clonazepam , a benzodiazepine tranquiliser
slow wave sleep problems
sleep walking (somnambulism) night terrors (pavor nocturnus) bedwetting (nocturnal enuresis)
most frequently occur in children and all have hereditary elements
somnambulism
disorder of arousal
person can engage in complex behaviours
pavor nocturnus
anguished screams, trembling, a rapid pulse, usually no memory for what caused the terror
bedwetting
10% of 7 year olds
fatal familial insomnia
neurodegenerative condition caused by damage to the thalamus
prion disease
symptoms of fatal familial insomnia
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.
