task 6 Flashcards
sleep is controlled by 3 groups of factors
- homeostatic factors:
> if we don’t sleep we feel sleepy
> we sleep longer to make up our ‘sleep dept’
> primary mediator: presence / absence of dopamine - allostatic factors:
> we stay awake in ‘dangerous situations’
> stressful events in environment
> primary mediator: hormonal & neural responses to stressful situations / neuropeptides involved in hunger & thirst - circadian factors: tend to restrict our period of sleep to a particular portion of day / night cycle
recuperation theory
> being awake disrupts homeostasis of body -> sleep required t restore it
implies that:
- sleepiness is triggered by deviation from homeostasis caused by wakefulness
- sleep is terminated by a return of homeostasis
evidence for this theory:
- greater levels of hormone secretion occur during stage 4 -> assists in repair of damaged tissues / cells
- ill people often sleep more -> indicating that sleep assists recovery
homeostasis
The process by which the body’s substances and characteristics (such as temperature and glucose level) are maintained at their optimal level.
theories of functions of sleep
- recuperation theory
- adaptation theory
- information consolidation theory
- clean-up theory
- sleep and learning
adaptation theory
sleep is result of internal 24-hour timing mechanism (not a reaction to disruptive effects of being awake)
> suggests sleep is like reproductive behaviour: we are highly motivated to engage it but it is not necessary to stay healthy
> support for theory: comparative research of different animal species
- animals with few natural predators (bears / lions) often sleep between 12 to 15 hours each day
- animals with many natural predators have short periods of sleep (between 4 or 5 hours)
=> sleep does not serve any specific function; just adaptation to our internal circadian rhythmic clocks
clean-up theory
sleep allows brain to clean itself up
> suggests that while asleep brain cleans itself of toxins & waste produced during the day
- when asleep, fluid flow through brain increases
-> waste disposal system: it cleans out the brain of waste products
information consolidation theory
based on cognitive research
> suggests that people sleep to process information that has been acquired during day
> sleep allows brain to prepare for the day to come
> sleep helps cement things we have learned during day into long-term memory
> support for this theory:
- sleep deprivation studies demonstrated that a lack of sleep has a serious impact on ability to recall and remember information
sleep and learning
sleep aids in the consolidation of long-term memories
=> hippocampus plays essential role
> REM sleep facilitates consolidation of non-declarative memories:
- gained through experience and practice
- those do not involve attempt to ‘memorise’ information
> SWS sleep facilitates consolidation of declarative memories:
- those that people can talk about (e.g. memories of past episodes of live)
- > brain appears to rehearse newly learned information during slow-wave sleep
structures within the brain that are involved in sleep
> hypothalamus > brain stem > thalamus > pineal gland > basal ganglia > amygdala
hypothalamus
contains groups of nerve cells that act as control centres affecting sleep and arousal:
> anterior hypothalamus including part of basal ganglia:
- promoting sleep
> posterior hypothalamus including part of midbrain:
- promoting wakefulness
> suprachiasmatic nucleus (SCN):
- clusters of thousand of cells that receive information about light exposure directly from eyes & control our behavioural rhythm
if damaged:
> people sleep throughout the day
- they are not able to match their circadian rhythms with the light-dark cycle
-> blind people maintain some ability to sense light and are able to modify their sleep cycle
brain stem
communicates with hypothalamus to control transitions between wake & sleep
> brainstem includes structures like pons / medulla / midbrain
reticular formation:
projects axons to brain that activate it
> electrical stimulation here promotes wakefulness & alertness
> also controls REM sleep
- low levels (of axons) produce sleep; high level produce wakefulness
if damaged:
> produces constant sleep states
reticular REM-sleep nuclei:
> REM sleep is controlled by nuclei pattered throughout the caudal reticular formation
> each site is responsible for controlling one of the major indices of REM sleep
> pons triggers REM-sleep
- large lesions abolish REM sleep
- electrical stimulation of this region can induce or prolong REM sleep
=> subcoeruleus: region of the pons where some neurone are active only during REM
brain stem and hypothalamus produce GABA:
- acts to reduce activity of arousal centres
brain stem plays role in REM sleep:
- sending signals to relax muscles essential for body posture and limb movements -> we don’t act out our dreams
thalamus
acts as relay for information from the senses to cerebral (= interprets & processes information from short to long-term memory)
> during most stages of sleep: thalamus is ‘quiet’ -> lets us tune out of external world
> during REM sleep: thalamus is active -> sending the cortex images / sounds / other sensations that fill our dreams
pineal gland
located within brain’s two hemispheres
> receives signals from SCN & increases production of hormone melatonin
- it helps us sleep once lights go down
> blind people can stabilise their sleep patterns by taking small amounts of melatonin
- peaks of melatonin over time are important for matching the body’s circadian rhythm to the external cycle of light and darkness
basal ganglia
near the front & bottom of brain promotes sleep & wakefulness,
while the part of midbrain acts as an arousal system
> release of adenosine from cells in the basal forebrain and other regions supports our sleep drive
- caffeine counteracts sleepiness by blocking the actions of adenosine
amygdala
almond-shaped structure involved in processing emotions
> becomes increasingly active during REM-sleep
reciprocal inhibition
between wake-promoting neurones & sleep-promoting neurones
> areas of brain that maintain wakefulness by activating the cortex also inhibits VLPO neurones
> VLPO neurones fire rapidly and induce sleep
- also inhibit activity in arousal centres
ventrolateral preoptic area (VLPO)
contains neurones that connect directly to the many arousal-promoting centres
> rather than stimulating activity in these areas, signals from VLPO neurones inhibit their activity
> by shutting down arousal centres VLPO promotes sleep
> majority of sleep neurones are located in this area
slow-wave sleep:
occurs when neurones in VLPO become active
> these neurones inhibit the systems of neurones that promote wakefulness
> in turn VLPO is inhibited by the same wakefulness.promoting regions
=> forming a kind of flip-flop that keeps us either awake of asleep
- when flip-flop is in ‘wake’ state: arousal systems are active and VLPO is inhibited
- when flip-flop is in ‘sleep’ state: VLPOA is active & arousal systems are inhibited
-> sleep neurones secrete inhibitory neurotransmitter GABA
REM- sleep:
controlled by another flip-flop
> only when sleep / awake flip-flop is in ‘sleeping state’ can REM flip-flop switch to REM state
> advantage of flip-flop: acts quickly
> disadvantage of flip-flop: can be unstable
if damaged:
> VPLOA neurones suppress sleep and the activity of these neurones increases during sleep
measuring sleep
system is called polysomnography (PSG):
- EEG: electrical recording of major changes in Brian during course of night’s sleep
> is used because EEG signals associate with being awake are different from those found during sleep
> different stages during sleep can be measured with EEG - EMG: electrical recording of muscle activity
> is used because muscle tone also differs between wakefulness and sleep
> EMG differences within sleep depending upon the stages of sleep - EOG: electrical recording of eye movements during sleep
> helps identify REM during which we often dream
> eye balls make characteristic movements that show us when someone is in this type of sleep
stages of sleep
definitions
non-REM sleep (nREM):
> stages of sleep without REM
> in humans, divided into stage 1 / 2 / 3
beta activity:
> EEG activity seen in wakefulness, comprising mix of many different high frequencies with low amplitude (= desynchronised EEG)
desynchrony:
many different neural circuits in brain are actively processing information
> occurs when person is alert & attentive to events in environment or is thinking actively
alpha rhythm:
brain potential that occurs during relaxed wakefulness
> consists of regular, medium-frequency waves
> the spent in alpha rhythm decreases as sleepiness increases -> smaller amplitude & irregular frequency
> vertex spikes: sharp-wave EEG pattern that is seen during stage 1 slow-wave sleep
