Sleep and Wakefulness Flashcards
Compare
Awake, REM sleep and NREM sleep
Awareness, Cerebral Cortex active
Unconscious, Cerebral Cortex active, Paralysis of muscles
Unconscious, Cerebral Cortex inactive, reduced muscle tone
Give all names of the sleep stages and which is higher proportion
N1 - Light sleep ‘transition’
N2
N3 - Slow Wave sleep - higher proportion of SW at the start
REM - higher proportion of REM at the end
Wakefulness
Muscle activity across Stages
Tonic - N1 N2 N3 (w decreasing activity, N3 weakest)
REM - Paralyzed
Eye activity across Stages + Wake
N1 - Decreased N2 - NO Eye N3 - Delta activity from EEG REM - Rapid eye movements Wake - More than REM
EEG Waves across Stages + Wake
N1 - decreasing alpha, increase theta (lower frequency) 4-7Hz
N2 - Theta; Sleep Spindles, K-Complexes
N3 - Delta (less than 4Hz)
REM - mixed frequency, Theta and Gamma; no alpha
Wake - Alpha, high freq (higher frequency) 8-12 Hz
So wavelengths go from
Alpha - Theta - Delta in decreasing frequency
Neurochemistry involved in REM
Activating: Ach!
- although Ach is wake-promoting by inhibiting VLPO during wakefulness; it is present during REM
Ventrolateral preoptic nucleus // Arousal System
Inhibitory: Monoamines like Histamine, Serotonin, Norepinephrine
Compare stages of sleep between young and old
Young: More REM, More Slow Sleep
Old: More awake, More Stage 1, 2,
Describe and explain 2 biological factors affecting sleep timing
Homeostatic Sleep Drive: builds up during wakefulness
- could be partially due to adenosine
- adenosine build up awake, decrease when sleep
- adenosine then VLPO GABA
Circadian: 24hr sleep cycle in the body
- caused by projections from SCN to brain stem
- environmentally influenced by light, circadian photoreceptor Melanopsin involved
Name sleep-promoting neuron in the anterior hypothalamus and its function
Ventrolateral Preoptic Nucleus, anterior hypothalamus
- produces GABA
- GABA is inhibitory; blocks wake-promoting areas
- activated by Adenosine and PG D2
- inhibited by Noradrenaline, Ach
Note wake-promoting and sleep-promoting have mutual inhibition;
What 2 affects of somnogen PG D2
Increase GABA - inhibitory, sleep-promoting
Increase Adenosine - sleep-promoting
Name highest functioning neuron types in awake and sleep
How about Ach? And Orexin
Awake: Monaminergic cell groups - Amines
Sleep: VLPN - GABA
Ach is high in awake, high in REM too but low in NREM
Orexin is Wake-promoting hence low in sleep
- orexin stabilizes arousal system
Pathophysiology of Narcolepsy, Type 1
Lack of Orexin, wake-promoting, in the brain due to cell destruction
Whats SCN function and what happens in SCN lesion
suprachiasmatic nucleus (SCN) - also in Hypothalamus - Loss of circadian rhythm; projection to BS lost
Note SCN do not have projections to VLPO directly but still links to other GABA, sleep promoting neurons. (wiki)
What is chronic snoring an indicator of
Obstructive Sleep Apnea
Give symptoms of Narcolepsy
Excessive daytime sleepiness; frequent sleep attacks
- also increased waking up at night
- sleep paralysis
Cataplexy: sudden loss of muscle tone when awake
Name the Inhibitory Neurotransmitters
Name the Arousal Neurotransmitters
their functions linking to VLPO and Arousal system
Sleep-Promoting
- Adenosine, PG D2
- GABA from Ventro-Lateral Preoptic Nucleus VLPO
- Activate VLPO and inhibit arousal system
Arousal, Wake-Promoting
- Orexin (may not be linked to VLPO)
- Monoamines: Histamine, Serotonin, Adrenaline
- Caffeine
- Ach
- Inhibit VLPO and activate arousal system
Acetylcholine is wake-promoting; also induces REM sleep