Lecture - Sleep Physiology Flashcards
1
Q
All animals sleep
A
- sleep habits, places nd posture vary
- some animals are nocturnal
- dolphins can sleep one hemisphere at a time
2
Q
Sleep is needed: sleep and adverse effects
A
- after 17-18 hours awake, performance is comparable to a BAC of 0.05
- with prolonged wakefulness, lapses or microsleeps are inevitable, eventually
- very LOW or HIGH hours of sleep are associated with mortality and morbidity
3
Q
DEtermining sleep
A
- behavioral
- electographic
- neuronal state
4
Q
EEG-defined sleep staging
A
- slowing and increased synchronization with deeper sleep
- sleep organised in cycles of 90-120 min
- NREM: increasing EEG slowing as light sleep transitions to deep sleep. Thalamus mediated greater disengagement of cortex from external inputs
- it is difficult to wake someone from SWS
- REM: EEG resembles quiet wakefulness or N1 with atonia and intermittent eye movement
5
Q
Homeostatic regulation of sleep
A
- sleep is a homeostatic phenomenon
- pressure for sleep increases with increasing time awake
- this is discharged with sleep
- this is called process S
6
Q
- Circadian regulation of sleep
A
- sleepiness is also determined by the time of day
- this is called process C: drive to maintain wakefulness
7
Q
Combined effects of process S and C
A
- S buolds across the waking hours
- circadian-determined drive to maintain wakefulness counteracts this for much of the daylight hours
- as process C wanes, we prepare for sleep
- during sleep, homeostatic sleep drive is discharged
- circadian drive falls off, helping maintain sleep across the night
8
Q
Basis of homeostatic drive
A
- adenoside accumulation in basal forebrain and other areas
- related to brain energy use
- adenosine acts on A1 receptors, decreaseing neuronal acrtivity and thus energy consumption
- adenosine accumulates in cat basal forebrain with prolonged wakefulness
- caffeine antagonises adenosine receptors
- but likely there are other mechanisms
9
Q
Synaptic homeostasis hypothesis
A
- connections are made when awake and are trimmed during sleep
- strongest connections are preserved
10
Q
What controls the circadian system?
A
- the Suprachiasmatic nucleus (SCN) of anterior hypothalamus
- autonomous oscillation, period 24.2 h
- BMAL1 and clock genes activate expression of Per and Cry
- Per and Cry translocate to nucleus, suppress BMAL1 and CLOCK
- inputs from retinal ganglion cells to SCN
- light and melatonin synchronize the circadian rhythm
11
Q
SCN outputs
A
- projection to cortex via multi-synaptic connections
- pineal gland melatonin section: synchronization of clocks in other organs
- regulate sleep/wake, REM sleep, feeding, metabolism, hormones
12
Q
Melatonin and temperature rhythm
A
- melatonin goes up
- temperature goes down
13
Q
Resynchronizing the clock: phase response curve
A
- bright light in evening will induce a phase delay, shifting bed time later
- morning bright light will cause phase advance
14
Q
Wake promoting systems
A
- cholinergic: acetylcholine
- monoaminergic: dopamine, histamine, serotonin, noradrenaline
- orexin
15
Q
Sleep-promoting neurons inhibit wake-promoting centres
A
- GABA and galanin
16
Q
The flip flop sleep switch
A
- wake centres inhibit sleep centres and vice-versa
- orexin maintains stability of wake state
- homeostatic and circadian system influence the switch
17
Q
Pharmacotherapeutic applications: sleep promoters
A
- benzodiazepine: enhance effect of GABA
- antihistamine that cross blood-brain barrier
- Suvorexant: orexin antagonist
18
Q
Wake promoters: pharmacotherapeutic
A
- Dexamphetamine: promote monoamine release
- pitolisant (presynaptic H3 inverse agonist): increase brain histamine levels, tested for narcolepsy
19
Q
DEvelopmental changes in sleep
A
- in the first year of life, sleep often starts with REM
- NREM sleep stages emerge over 2-6 months of life
- SWS maximal in young children, decreases with age
- arousals increase in frequency with age, so sleep is less consolidated
