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
how does the pons control sleep?
- 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
how does the reticular formation control sleep?
- 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
how does the raphe nucleus control sleep?
- 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
what happens to sleep if we cut the spinal cord behind or after the pons?
- 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
how do the peribrachial area of the pons and acetylcholine control sleep?
acetylcholine and peribrachial area are responsible for brain wave patterns that look like we are awake when we are in REM
30
how do norepinephrine systems affect sleep?
- 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
how do general anesthetics work to cause sleep?
- 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
how do hypnotics (sedatives) work to cause sleep?
- 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
what are some problems with the use of benzodiazepines?
- 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
what other substances work similarly to benzodiazepines? how do they work?
- alcohol works on a similar mechanism, also decrease REM sleep
- alcohol and benzo can work together to cause death
35
how do serotonergic drugs affect sleep?
serotonergic drugs are not effective in treating insomnia, but increasing the brains serotonin precursors (tryptophan) can aid in sleeping
36
how do antihypnotics (stimulants) affect sleep?
- promotes the release of catecholamines (dopamine, NE)
- increases wakefulness and alertness but almost completely suppresses REM
- some can be addictive
37
how does caffeine affect sleep?
- 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
what is narcolepsy?
- 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
what are some potential causes of narcolepsy?
- 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
what are some potential treatments for narcolepsy?
- norepinephrine and serotonin agonists to reduce attack
- development of orexin-like drugs
