Neural basis of sleep Flashcards
How is sleep measured?
sleep lab
go to peoples home
measure electrical brain activity via EEG (electroencephalogram)
measure eye movement during sleep via EOG (electrooculogram)
measure muscle activity (chin or legs) - useful identifying sleep disorder via EMG (electromyogram)
–> collectively they’re called polysomnography = objective measure used to study sleep
often accompanied with sleep survey
states of arousal in sleep
4 bands
EEG looks at which characteristics of wave?
EEG - we have different brain oscillations when we’re awake and when were asleep
1 - beta waves: >13Hz (highest frequency) // < 5mv (lowest amplitude)
2 - alpha waves: 8 - 13Hz // 5-15mV
3 - Theta: 4- 7 Hz // 10 - 50mV
4 - Delta: < 4Hz // > 50mV
- we use this to distinguish between stages of sleep
= 4 key bands when measuring sleep
- EEG looks at frequency of these waves (how often they occur) and amplitude (size of the brain oscillation )
- only because of EEG we’ve come to realise there are many stages and differences within sleep
2 components of sleep
1) REM = only identified when EOG was used (Showed rapid eye movement)
2) NREM = within non-REM there are 4 stages (1-4)
stages 3 + 4 are known as slow wave sleep (due to electrical brain activity they show)
- sleep becomes ‘deeper’ as you move 1 - 4
Awake brain
BETA activity
= high frequency
when we relax = alpha (amplitude increases, frequency decreases)
stages 1 - 4
1 = very light stage of sleep initially, body is getting prepared for sleep (easily woken up) = THETA
relaxed state, heart rate drops. slight drop in body temp, muscles start to relax (not paralysed)
(4-5%)
2 = start to see spindles and k-complexes
sleep spindles = rapid burst of activity that originate in thalamus and project onto cortical regions in brain (shown to play big role in memory consolidation)
body trying to stop anything external from waking you up (helps gradual transition to deep sleep)
(45-55%)
3 + 4 = start to see big changes in oscillations, delta activity (lower frequency and larger amplitude), ‘slow wave sleep’, children often have night terrors during this stage (so when they wake up = feel groggy and often confused), v important in memory consolidation, older population tend to struggle initiating and maintaining this deep sleep (may explain why they have problems with memory)
(3 = 4-6%)
(4 = 12-15%)
REM
activity looks very similar to waking brain
dreams and nightmares
EOG - rapid eye movement detected
EMG will show v little activity as we are paralysed during this part of sleep (loss of muscle tone)
REM behavioural disorder = don’t have muscle tone and act out their dreams
process a lot of emotions (managing and processing emotions) = why we dream?
our way of processing emotions we have felt during the day (often dreams are quite emotionally charged)
(20-25%)
Sleep cycle
hypnogram shows sleep stages
- 1st couple of hours in deep sleep
1 cycle = through all stages into REM
typically have around 5 cycles in one night (each cycle is around 90 mins)
deeper stages of sleep earlier in the night, and REM at the end (dream more at the end of the night)
if you sleep late you can miss the deep stages of sleep because you’re out of your normal rhythm = don’t feel refreshed after
might wake up in the night (usually after REM as brain activity is similar to awake brain)
–> won’t remember waking up because you still remain in sleep like state
How do we know when to sleep?
2 components
other key component?
Define Dinural and nocturnal
1) Circadian rhythm = biological rhythm. It is a function of living organisms that display a rhythm of about 24 hrs
DINURAL = active during the day
NOCTURNAL = active during the night
2) Sleep homeostasis (sleep pressure) = works with circadian rhythm
refers to our need to sleep (accumulates throughout the day)
MELATONIN =secreted by pineal gland which produces feedback to the master clock –> melatonin is the biological representation of the dark (secreted over night = as it increases as does the need to sleep)
- light blocks the production of melatonin = wake up in the day
(SCN controls the production of melatonin)
Circadian clock and sleep-wake regulation
SCN (Moore, 2007)
How do we research SCN?
deep in the brain we have the suprachiasmatic nucleus (SCN) which is our internal body clock/ representation of time
(location = where optic nerve crosses = optic chiasm)
- the SCN is the ‘masterclock’ and ensures we maintain a 24hr rhythm for numerous processes eg. sleep/ hormones/ temp (Moore, 2007)
If we dissect the SCN we see neurons - all the cells have a 24hr rhythm of activity = how we regulate sleep and wake patterns
SCN also manages other processes that follow a 24hr rhythm:
-hormone secretion
-appetite control
-muscle repair
SCN lesioned animals can’t regulate their 24hr rhythm = sleep-wake pattern completely gone
How do we reset this clock?
- if blind?
LIGHT
= main cue to synchronize the master circadan oscillator (Domien, 2007)
(note: intensity of light also appeared to be important)
so, when we get jet lag, this is because out internal clock is out of sync with the external cues (light = trigger)
- Zaidi et al (2007) - if someone is blind, how do they reset?
often, people are blind due to damaged rods and cones. These peoples sleep-wake cycles can be maintained as the photosensitive retinal ganglion cells are still able to function and gain info about local time (sensitive to blue light)–> because of a pigment called melanopsin which is activated by blue light
Sleep homeostasis
- role of adenosine
as homeostatic drive for sleep accumulates = circadian drive for arousal decreases
in day = sleep pressure builds up and overtakes circadian drive
asleep = need to sleep decreases, this builds up again during the day
with increasing homeostatic drive there is an increase in firing of neurons in the ventrolateral preoptic nulceus (GABA and Galanin released from here and inhibit excitatory transmitters
(Moore, 2007)
ADENOSINE:
- during the day when your brain is active = uses a lot of energy (energy in form of ATP and broken down into adenosine = sleep pressure)
- high levels of adenosine at night (sleep pressure) due to less ATP (broken down)
Neurotransmitters involved in sleep: (regulating sleep-wake pattern)
serotonin noradenalin histamine dopamine acetylcholine = EXCITATORY
galanin
GABA
= INHIBITORY
hypocretin (orexin)
=NEUROMODULATOR
looking at neurological/ psychiatric conditions, all of them involve some of these NETs, and disorders often involve problems with sleep = shows these neurotransmitters really help to govern sleep
Ascending arousal system/ reticular activating system
basal forebrain and pons region are critical for arousal
- it requires coordinated activity of interconnected ascending arousal system
-EXCITATORY NETs (Wake-promoting)
acetylcholine (from LDT to PPT) - sends signals to thalamus
dopamine/ histamine/ noradrenalin/ serotonin = all innervate cortical regions and send signals to cortex
(antihistamines can therefore cause sleepiness)
-NEUROMODULATORS (wake-promoting)
hypocretin = syntheses in a small group of cells in the lateral and posterior hypothalamus
-INHIBITORY system (sleep-promoting)
located in the ventrolateral preoptic area (VLPO) of the hypothalamus = key area for inhibiting (GABA & Galanin)= inhibit excitatory (active during sleep)
(Schwartz & Roth, 2008)
hypocretin stablilizes sleep wake states = neuromodulator involved in flipping the sleep-wake switch
–> those with narcolepsy have a depletion of hypocretin
Sleep-wake switch
1) wakefulness = neurotransmitters (5 excitatory) ACTIVE. Stabilised by neuromodulator (hypocretin)
- -> blocks inhibitory NETs ( GABA and Galanin)
2) sleep = inhibitory ACTIVE (GABA and Galanin)
- blocks wake-active NETs
- blocking hypocretin = can no longer modulate wake promoting NETs = can’t stay awake
How is hypocretin affected/linked to sleep pressure?
build up of adenosine ends up blocking hypocretin (=can’t modulate wake-promoting NETs, so they’re less active)
-sleep active NETs become more active = transition from wake to sleep
