Task 1 Flashcards
Adenosine
-Carlson
- primary role in control of sleep
- caffeine blocks adenosine receptors, preventing inhibitory effect on neural activity and reducing the effects of sleep deprivation
- astrocytes maintain small stock of nutrients in form of glycogen –> increased brain activity this glycogen converted into fuel for neurons
- prolonged wakefulness causes decrease glycogen in brain –>causes increase extracellular adenosine –> inhibitory effect on neural activity = sleep promoting substance
- SWS neuron in brain rest, astrocytes renew their stock of glycogen
acetylcholine
-Carlson
- role in arousal
- two groups (one in pons and one in basal forebrain) produce activation and cortical desynchrony when stimulated
- third group (in medial septum) controls activity hippocampus
- acetylcholinergic agonists increase EEG signs of cortical arousal, antagonists decrease them
- high during waking, low during SWS and high during REM
norepinephrine
-Carlson
- located in locus coeruleus in dorsal pons
- arousal and sleeplessness mediated by noradrenergic system of the LC
- firing rate high during wakefulness and zero during REM and low during SWS
- activity of noradrenergic LC neurons increase animals vigilance
serotonin
-Carlson
- plays role in activating behaviour
- serotonergic neurons found in raphe nuclei–> causes locomotion and cortical arousal
- located in medullary and pontine regions of reticular formation
- higher when awake, low while REM, middle while SWS
- PCPA reduces cortical arousal –> drug that prevents the synthesis of serotonin
Histamine
-Carlson
- plays role in wakefulness and arousal
- located in the tuberomammillary nucleus (TMN) of the hypothalamus
- high during waking, low during SWS and REM
Orexin
-Carlson
- degeneration of orexinergic neurons cause of narcolepsy
- located in lateral hypothalamus
- high during waking, low during SWS and REM
Neural control of SWS
- 3 types
- Carlson
- Homeostatic factor
- ->missing sleep, sleep longer to make up for our sleep dept
- ->presence (waking) or absence (sleeping) of adenosine
- Allostatic factor
- ->reactions to stressfull events in environment to override homeostatic control
- ->mediated by hormonal and neural responses and by neuropeptides (orexin) that are involved in hunger
- Circadian factor
- ->restrict period of sleep to day/night cycle
Neural control of SWS
- preoptic area
- Carlson
- preoptic area located in anterior hypothalamus involved in control of sleep
- preoptic neurons (sleep neurons) active –> suppress activity arousal neurons, we fall asleep
- sleep neurons located in the ventrolateral preoptic area (vlPOA)
- sleep neurons inhibited by histamine, serotonin and norepinephrine
Neural control of SWS
- flip-flop
- Carlson
- sleep neurons are active and inhibit the wakefulness neurons or the wakefulness neurons are active and inhibit the sleep neurons
- GABAergic neurons connect sleep-promoting regions and wakefulness promoting regions
- wake state–> arousal systems active and sleep-promoting regions are inhibited
- advantage–> switches quickly, problem they can be unstable
Neural control of SWS
- orexinergic neurons
- Carlson
- function is to help stabilize flip-flop through their excitatory connections to wakefulness neurons
- receive excitatory signal from biological clock that controls rhythm of sleep and waking
- receive hunger related signals and activate orexinergic neurons, satiety related inhibit them
- activation holds flip-flop on
- motivation to remain awake
Role adenosine in sleep/wake transition
-Carlson
- adenosine produces drownsiness and sleep
- increased during wakefulness and decreas during sleep
Stages of sleep
- waking
- Carlson
- Alpha activity –> regular, medium frequency waves, produced when person is resting quietly, eyes closed
- beta activity –> irregular, low-amplitude waves, desynchronized activity (alert or attentive to events in environment)
Stages of sleep
- stage 1 NREM
- Carlson
- theta activity –> becoming more synchronized
- transition between sleep and wakefulness
- hypnic jerks –> muscle contractions followed by relaxation
Stages of sleep
- stage 2 NREM
- Carlson
- Sleep spindles –> short burst of waves 2-5 times/min, role in consolidation of memory
- K complexes –> sudden, sharp waveforms
- if wakaned might report not sleeping
Stages of sleep
- stage 3 NREM
- Carlson
- Slow-wave sleep
- delta activity –> high amplitude
- deepest stage
- when awakend, groggy and confused
Stages of sleep
- REM
- Carlson
- when awakend person alert and attentive
- EEG desynchronized with theta activity and beta activity
- eyes are rapidly moving, loss of muscle tone
- narritive dreams
- cerebral blood flow and oxygen consumption accelerated
- genitals active
Stages of sleep
-Carlson
- 90 min with REM voor 20-30 min
- most SWS during first half of the night
Two process model
- what is it
- Manber
- explains regulation of sleep
- homeostatic process S (sleep drive)
- circadian process C (circadian clock)
- interaction determines the likelihood that sleep will occur
- ideal time –> sleep drive is high, Process C on decline, Process S is stronger then Process C
Two process model
- homeostatic process S
- Manber
- body’s drive for sleep
- sleeping decreases the sleep drive
- related to NREM, N3 sleep
- dominates first third of night when sleep drive is highest
Two process model
- circadian process C
- Manber
- represents biological clock
- alerting signals lowest 1-3 hours prior to habitual morning wake time, increase accross day
- synchronisized with core body temperature and melatonin secretion
- related to REM sleep, dominates second half night
Sleep architecture
-Manber
- the electrophysiological structure of sleep
- objective measurement based on polysomnography (PSG)
- all stages unique patterns
- sleep begins with N1, N2, N3 and then REM –>first sleep cycle
Measurements of sleep
- polysomnography
- Manber
- gold standard of objective sleep measurement
- measuring electrical activity brain (EEG), muscle tones around eyes (EOG), chin and legs (EMG) and breathing patterns
- minutes to fall asleep (SOL; sleep onset latency)
- number en times awakenings (WASO; wake after sleep onset)
- sleep efficiency = 100 x (TST/TIB)
- TIB; time in bed
- TST; total sleep time = TIB-(SOL+WAS))
Measurements of sleep
- actigraphy
- Manber
- based on movement of wrist
- cannot provide info about sleep stages
Measurements of sleep
- subjective measurements
- Manber
- sleep diaries and sleep questionnaires
- economical and practical
Measurements of sleep
- daytime sleepiness
- Manber
- Multiple sleep latency test (MLST)
- ->physiological sleepiness
- ->propensity to fall asleep, napping
- ->score less than 5 min excessive sleepiness
- Maintenance of wakefulness test (MWT)
- ->dark room instructed to stay awake
- ->higher MWT reflects higher alertness
Sleep homeostasis
- what is it
- Tobler
- basic principle of sleep regulation
- regulated by Process S, Process C and their interacton
- Process S regulates sleep intensity
- Process C regulates timing of sleep
Sleep homeostasis
- sleep deprivation
- Tobler
- sleep deprivation major effects process S, no effect on process C
- sleep deprivation leads to increase slow-wave activity
- person 2h nap lower levels slow-wave activity during subsequent night sleep
- Process S is deficient in depression
Macro sleep structure changes aging
-Mander
- advanced sleeping time
- longer sleep onset latency
- shorter sleep and more fragile and more awake
- increased fragmentation
- reduced SWS, increased lighter NREM
- shorter and fewer NREM-REM cycles
- increased daytime naps
Slow waves changes aging
-Mander
- Slow-wave activity bound with homeostatic drive
- SWA hightest first NREM declines across NREM cycles=homeostatic dissipation of sleep pressure
- homeostatic increases in SWS time and SWA blunted in older= impairment homeostatic regulation of SWA in older adults
- amplitude and density of slow waves reduced in older
- mean frequency slowing in average frequency in older
Sleep spindles changes aging
-Mander
- density declines as adult age
- same amount of NREM sleep time, still differences in density and amplitude of slow-waves can be observed
Sleep structure and stages changes aging
-Mander
- LHA and LC maintain stable periods of wake
- POA maintain stable sleep
- SCN modulates orexigenic activity
- strength of sleep and wake signal compromised resulting in unstable brain state
- older show reduced galanin expressing POA neurons, reduced orexin expressing in LHA, reduced responsivity in LC
- decreased sleep duration, increased sleep latency, increased number of sleep stage transition, greater fragmentation of consolidated periods of sleep and wake
homeostatic sleep drive changes aging
-Mander
- extracellular adenosine higher in older
- loss of adenosine A1 receptors –> decrease sensitivity to the higher extracellular adenosine
sleep oscillations changes aging
-Mander
- structural brain atrophy is mechanism age related impairments
- atrophy in PFC predicts impairment NREM slow wave
- deficit NREM slow wave amplitude and density associated with reduced grey matter volume and thickness
sleep, aging and memory
-Mander
- impairment in spindle density predicts failure hippocampus in episodic associative memory encoding next day
- NREM fast sleep spindles support memory encoding, disruption weaken the hippocampal encoding and thus the sleep-dependent learning restoration
- NREM slow waves support offline consolidation of new memories promoting hippocampal-neocortical memory transformation, impairment predict worse overnight hippocampal neocortical memory transformation
Sleep quality and aging
-unruh
- older associated with shorter sleep time, diminished sleep efficiency and more arousal
- older men more stage 1 and 2 sleep, less SWS and REM and significant but smaller change women in stage 2 and REM
- subjective sleep quality declined with age in women
- women more trouble falling asleep and waking up early of during night
- poorer sleep according PSG in men
- poorer sleep according subjective report in women
Sleep duration recommendation
-Hirschkowitz
- newborns 0-3 months - 14-17h
- infants 4-11 months - 12-15h
- toddlers 1-2 year - 11-14h
- prescholers 3-5 year - 10-13h
- school aged 6-13 year - 9-11h
- teenagers 14-17 year - 8-10h
- young adults and adults 18-64 year - 7-9h
- older adults >65 year - 7-8h