Sleep Flashcards
1
Q
what is the energy conservation theory of sleep? what is some evidence for and against the theory?
A
- we sleep to conserve energy because we use slightly less energy when we sleep
- evidence for: smaller animals with higher metabolic rates (use more energy) sleep more
- evidence against: we still use energy when we sleep, not that much saving
- meat eating animals don’t show as much of a correlation between mass and amount of sleep
2
Q
what is the body/brain restoration theory of sleep? what is some evidence for and against the theory?
A
- being awake disrupts homeostasis and sleep can be time for the body to repair itself
- evidence for: growth hormones are released during sleep
- sleep helps recovery from illness
- prolonged lack of sleep can be fatal
- brain removes more waste product during sleep
- evidence against: intense metabolic expenditures during day do not reliably increase amount of sleep needed, only decreases time to fall asleep
3
Q
what is the memory consolidation theory of sleep? what is some evidence for the theory?
A
- sleep helps us remember information learned during waking
- evidence for: sleep deprivation can disrupt memory retrieval, humans have better verbal memory retention and motor memories if tested following sleep
4
Q
what are the active and passive theories of memory consolidation and sleep?
A
- passive: waking interferes with memory retention, or sleeping slows down memory degradation
- active: sleep processes are actively involved in storing memories
5
Q
what evidence supports the active role of sleep in memory consolidation?
A
- we have more REM sleep after new learning
- increased activity in memory centres during sleep
- studies in rats suggest that temporal sequences of patterned activity linked to memory traces are reactivated during REM
6
Q
what are the current ideas on whether REM sleep is related to learning?
A
- REM sleep may aid in learning but may not be necessary for it
- debates on whether is improves consolidation (active) or diminishes irrelevant ones (passive)
7
Q
what are the four phenomenon that characterize sleep?
A
- reduced movement
- stereotypic posture
- reduced response to stimulation
- reversibility
8
Q
what are the different ways we can measure sleep in the lab?
A
- electroencephalogram (EEG): measures electrical activity of the brain
- electrooculogram (EOG): measures eye movements
- an electrode near the eye records change in voltage as the eye moves - electromyogram (EMG): measures electrical activity of the muscles
- usually recorded under the chin, muscle tone is a good reflection of the rest of the body
9
Q
what are the two main classes of stages of sleep?
A
- slow wave sleep
- rapid eye movement (REM) sleep
10
Q
how do brain waves look when we are awake?
A
- beta waves: fast frequency (15-20Hz) and low amplitude (10-30mV)
- when eyes close and relax, we have alpha waves (9-12 Hz)
- after a period, alpha waves decrease. waves become smaller and irregular and slower with random bigger spikes
- REMs are absent, but slow rolling eye movements appear
- EMG is moderate to low
11
Q
what does stage 2 sleep look like?
A
- EEG looks similar, but additional 12-14Hz burst of waves called sleep spindles are observed
- REMs are rare, EMG low to moderate
- period where you don’t think you’re asleep, but you’re not responsive to the environment
12
Q
what do stage 3 and 4 of sleep look like?
A
- delta waves: high amplitude (>75mV) and slow waves
- stage 3-late (stage 4) defined by delta waves at least 50% of the time
13
Q
how do we cycle through the stages of sleep?
A
- we cycle from stage 1-4, and then back to stage 2
- brain waves start to resemble stage 1/awake stages with low voltage and mixed frequency
- bursts of rapid eye movements appear, EMG is absent but you see occasional sleep
14
Q
what happens during REM sleep that doesn’t happen in slow wave sleep?
A
- increased and sustained cortical activity
- severely reduced neural responses to sensory stimuli
- vivid dreams
- complete loss of muscle tone, even though motor cortex is active
15
Q
how often do the sleep cycles repeat, and what are the cycles characterized by?
A
- over the course of one night’s sleep, cycle repeats 4-5 times
- 50% is stage 2 sleep, 20% is REM sleep
- one cycle takes 90-110 minutes
- early in sleep period, you see more stage 3 sleep, but as sleep progresses you see less stage 3, and longer REM episodes
16
Q
how does REM sleep affect dreaming?
A
- 80% report dreaming when awakened from REM while only 10% report dreams from slow sleep wave awakenings
- stage 2 awakenings sometimes reveal non-vivid thinking dreams
- external stimuli can sometimes influence dream, spray water on subject in REM, they dream of water falling on them
- dreams run on real time, don’t last a few seconds usually
- sleep walking and talking do not occur during REM sleep as core muscles tend to be totally relaxed
17
Q
what happens when a person is sleep deprived?
A
- some people display hallucinations and paranoia
- most show increased irritability and decreased ability to concentrate
- no real effects on IQ tests
- brain regions activated in rested subjected doing arithmetic problems are not active in sleep-deprived subjects
- more complex cognition mediated by the frontal lobes are most susceptible to sleep deprivation
- including innovative thinking, planning, selective attention, cognitive flexibility
- tasks with high motivation/arousal components are not as affected
18
Q
what are the major health consequences with extreme long-term deprivation?
A
- laboratory animals can die after about 19 days with no sleep
- humans with fatal familial insomnia die within 7-24 months of disorder
- autopsy shows degeneration in the brain but actual cause of death seems to be due to general disruption of immune function
- they don’t go through regular sleep cycles and aren’t able to fight off infections and pathogens during sleep
19
Q
how are the effects of sleep deprivation related to REM sleep?
A
- cognitive effects of sleep deprivation seem due to reduced REM sleep
- effects can be observed after a few nights of less than normal sleep
- waking subject from only REM sleep has similar consequences
- after repeated REM sleep deprivation, subjects have rebound increases in bouts of REM, meaning they have more REM when they get back into regular sleep cycle
20
Q
how is sleep altered after a period of sleep deprivation?
A
- following sleep deprivation, subjects try to make up sleep loss with more REM sleep
- sleep time increases for a few days
- more stage 3 sleep, at the expense of stage 2 sleep
- REM episodes become more frequent, are longer, and/or more intense, individuals become more efficient sleepers
21
Q
how much sleep do we really need?
A
- amount of sleep needed varies among people and with age
- older people spend less time in stage 3
- 8 hours may not be right for everyone, study showed those averaging 7 hours a night had the lowest mortality rates
- people sleeping more or less than 7 hours had higher mortality rates
- reducing sleep in short tern can have consequences, but if reduction occurs over prolonged period, there are fewer problems
22
Q
how does reducing sleep in the long term affect us?
A
- subjects reduced sleep time by 30 minutes every 2-4 weeks until they were at 4.5 hours
- showed no adverse effects
- increased efficiency of sleep, less time to fall asleep and less awakenings, and increased stage 4 sleep
23
Q
what are the main brain areas that control sleep?
A
- basal forebrain
- pons
- reticular formation
- raphe nucleus
24
Q
how does the basal forebrain control sleep?
A
- group of nuclei part of the hypothalamus
- regulates slow wave sleep
- some neurons in this area use GABA as neurotransmitters and release in the adjacent tubermamilliary nucleus
- slows the brain
- lesioning this area abolishes SWS
- stimulating basal forebrain induces SWS
25
Q
how does the pons control sleep?
A
- group of nuclei that regulate different aspects of REM
- brain activity patterns, shut down muscles (atonia)
- lesioning this area abolishes REM sleep
- stimulating this area activates REM sleep
- some neurons in this region are active oNLY during REM
- lesion in the subcoeruler nucleus leads to loss of uncoupling of motor systems during sleep
26
Q
how does the reticular formation control sleep?
A
- group of nuclei which regulate waking and arousal
- lesioning this area leads to persistent sleep
- stimulating this area leads to rapid awakening from sleep
- sends input to thalamus and is also connected with basal forebrain (keeps us awake by inhibiting basal forebrain)
27
Q
how does the raphe nucleus control sleep?
A
- sends serotonin inputs that inhibit reticular formation neurons
- group of neurons project to the reticular formation and can inhibit activity, leading to less wakefulness
- lesions of the raphe lead to insomnia
- raphe also projects to other regions that control REM sleep, like…
- peribrachial area in the pons: use acetylcholine to mediate REM
- group of serotonin neurons inhibit peribrachial neurons, decreasing REM sleep
- serotonin can help us come out of REM sleep and go into slow wave sleep
28
Q
what happens to sleep if we cut the spinal cord behind or after the pons?
A
- if we cut the spinal cord or right behind the pons…
- normal SWS and REM sleep
- sleep is controlled by the brain in front of the pons
- if we cut in front of the pons, we have constant slow wave sleep and no REM sleep
29
Q
how do the peribrachial area of the pons and acetylcholine control sleep?
A
acetylcholine and peribrachial area are responsible for brain wave patterns that look like we are awake when we are in REM
30
Q
how do norepinephrine systems affect sleep?
A
- neurons from locus coeruleus project to peribrachial areas
- norepinephrine inhibits neurons that mediate REM sleep
- NE projects widely through brain and cortex, also mediates arouse
- REM sleep episodes occue when neurons in the raphe and locus coeruleus decrease firing, so that peribrachial neurons can increase firing
31
Q
how do general anesthetics work to cause sleep?
A
- general anesthetics cause unconsciousness
- produce slow waves in EEG that resemble SWS
- almost all general anesthetics are agonists of GABA-A receptors
- supports idea that some brain system uses GABA to promote SWS
32
Q
how do hypnotics (sedatives) work to cause sleep?
A
- benzodiazepines act on GABA transmission
- are not direct agonists, but facilitate binding of GABA to the GABA-A receptor
- cause decrease in cortical activity
- when drug binds, it increases potency of GABA to open receptor channel but does not open channel if GABA is not also bound
- act as positive allosteric modulators
- it is not responsible for activating the receptors, but boosts inhibitory signals when it is activated
- it requires GABA to be activated
It will stay open longer and increase the inhibitory influence that the receptor has
33
Q
what are some problems with the use of benzodiazepines?
A
- tolerance and addiction develops
- can lead to insomnia when drugs are discontinued
- distort normal pattern of sleep, stay in SWS longer
- increases stage 2 sleep but decreases REM and stage 3 sleep
- has a hangover effect with REM rebound, makes us feel sleepy even after 10 hours of sleepw
34
Q
what other substances work similarly to benzodiazepines? how do they work?
A
- alcohol works on a similar mechanism, also decrease REM sleep
- alcohol and benzo can work together to cause death
35
Q
how do serotonergic drugs affect sleep?
A
serotonergic drugs are not effective in treating insomnia, but increasing the brains serotonin precursors (tryptophan) can aid in sleeping
36
Q
how do antihypnotics (stimulants) affect sleep?
A
- promotes the release of catecholamines (dopamine, NE)
- increases wakefulness and alertness but almost completely suppresses REM
- some can be addictive
37
Q
how does caffeine affect sleep?
A
- acts as an antagonist to adenosine
- adenosine is inhibitory transmitter distributed throughout the brain (cortex, reticular formation)
- adenosine accumulates with activity in the brain, decreases during sleep
- caffeine or theophylline from tea can block adenosine, increase arousal
38
Q
what is narcolepsy?
A
- sudden attack of sleep where people go directly from waking state to REM sleep
- attacks come on during periods of intense emotion
- loss of muscle tone (cataplexy) during attack
- regular sleep stages when they choose to go to sleep
39
Q
what are some potential causes of narcolepsy?
A
- disruption in neural circuits that mediate REM sleep
- gene that encodes for peptide neurotransmitter hypocretin (orexin) is involved
- people with narcolepsy lose 90% of all hypocretin neurons
- hypocretin projections from hypothalamus coordinate activity in sleep-centers (basal forebrain, reticular formation, locus coeruleus)
40
Q
what are some potential treatments for narcolepsy?
A
- norepinephrine and serotonin agonists to reduce attack
- development of orexin-like drugs
