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Sleep and sleepdisorders > Task 1 > Flashcards

Task 1 Flashcards

1
Q

Adenosine

-Carlson

A
  • 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
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2
Q

acetylcholine

-Carlson

A
  • 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
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3
Q

norepinephrine

-Carlson

A
  • 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
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4
Q

serotonin

-Carlson

A
  • 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
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5
Q

Histamine

-Carlson

A
  • plays role in wakefulness and arousal
  • located in the tuberomammillary nucleus (TMN) of the hypothalamus
  • high during waking, low during SWS and REM
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6
Q

Orexin

-Carlson

A
  • degeneration of orexinergic neurons cause of narcolepsy
  • located in lateral hypothalamus
  • high during waking, low during SWS and REM
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7
Q

Neural control of SWS

  • 3 types
  • Carlson
A
  • 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
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8
Q

Neural control of SWS

  • preoptic area
  • Carlson
A
  • 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
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9
Q

Neural control of SWS

  • flip-flop
  • Carlson
A
  • 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
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10
Q

Neural control of SWS

  • orexinergic neurons
  • Carlson
A
  • 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
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11
Q

Role adenosine in sleep/wake transition

-Carlson

A
  • adenosine produces drownsiness and sleep

- increased during wakefulness and decreas during sleep

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12
Q

Stages of sleep

  • waking
  • Carlson
A
  • 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)
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13
Q

Stages of sleep

  • stage 1 NREM
  • Carlson
A
  • theta activity –> becoming more synchronized
  • transition between sleep and wakefulness
  • hypnic jerks –> muscle contractions followed by relaxation
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14
Q

Stages of sleep

  • stage 2 NREM
  • Carlson
A
  • 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
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15
Q

Stages of sleep

  • stage 3 NREM
  • Carlson
A
  • Slow-wave sleep
  • delta activity –> high amplitude
  • deepest stage
  • when awakend, groggy and confused
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16
Q

Stages of sleep

  • REM
  • Carlson
A
  • 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
17
Q

Stages of sleep

-Carlson

A
  • 90 min with REM voor 20-30 min

- most SWS during first half of the night

18
Q

Two process model

  • what is it
  • Manber
A
  • 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
19
Q

Two process model

  • homeostatic process S
  • Manber
A
  • 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
20
Q

Two process model

  • circadian process C
  • Manber
A
  • 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
21
Q

Sleep architecture

-Manber

A
  • 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
22
Q

Measurements of sleep

  • polysomnography
  • Manber
A
  • 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))
23
Q

Measurements of sleep

  • actigraphy
  • Manber
A
  • based on movement of wrist

- cannot provide info about sleep stages

24
Q

Measurements of sleep

  • subjective measurements
  • Manber
A
  • sleep diaries and sleep questionnaires

- economical and practical

25
Q

Measurements of sleep

  • daytime sleepiness
  • Manber
A
  • 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
26
Q

Sleep homeostasis

  • what is it
  • Tobler
A
  • 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
27
Q

Sleep homeostasis

  • sleep deprivation
  • Tobler
A
  • 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
28
Q

Macro sleep structure changes aging

-Mander

A
  • 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
29
Q

Slow waves changes aging

-Mander

A
  • 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
30
Q

Sleep spindles changes aging

-Mander

A
  • density declines as adult age

- same amount of NREM sleep time, still differences in density and amplitude of slow-waves can be observed

31
Q

Sleep structure and stages changes aging

-Mander

A
  • 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
32
Q

homeostatic sleep drive changes aging

-Mander

A
  • extracellular adenosine higher in older

- loss of adenosine A1 receptors –> decrease sensitivity to the higher extracellular adenosine

33
Q

sleep oscillations changes aging

-Mander

A
  • 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
34
Q

sleep, aging and memory

-Mander

A
  • 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
35
Q

Sleep quality and aging

-unruh

A
  • 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
36
Q

Sleep duration recommendation

-Hirschkowitz

A
  • 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

Sleep and sleepdisorders (6 decks)

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