Task 6- Sleep Flashcards
EEG (Electroencephalography)
- Electrical recording of major changes in the brain during night’s sleep.
- EEG signals associated with being awake are different from those found during sleep
- can measure Different stages of sleep
EMG (Electromyography)
- Electrical recording of muscle activity
- used because muscle tone also differs between wakefulness and sleep.
- EMG differences within sleep, depending upon the stage of sleep
EOG
- Electrical recording of eye movements during sleep
- Very specific measurement that helps identify (REM)
- Eye balls make characteristic movements
alpha activity
IN WAKEFULNESS STAGE
- Smooth electrical activity
- associated with a state of relaxation.
beta activity
IN WAKEFULNESS STAGE
- Irregular electrical activity
- associated with a state of arousal
Theta activity
IN STAGE 1
- slower signals, smaller amplitude
- during early stages of slow-wave sleep and REM sleep
K komplexes
IN STAGE 2
sudden sharp waves
only during stage 2 sleep
triggered by noises
sleep spindles
IN STAGE 2
short bursts of waves (2-5 times a minute)
delta activity
IN STAGE 3,4(3)
-high amplitude, low frequency
wakefullness stage
- alpha activity
- beta activity
Stage 1 sleep
(NREM1)
- transition between sleep and wakefulness
- theta activity
- vertex spikes
- Eyelids from time to time slowly open and close and eyes roll up and down
theta activity in stage 1
firing of neurons is becoming more synchronised, slower signals, smaller amplitude
vertex spikes
sharp waves
Stage 2 sleep
(NREM2)
- higher amplitude, lower frequency
- sleep spindles
- k komplexes
Stage 3/4
(NREM3)
- slow wave sleep
- delta activity
- down state (inhibition period: resting)
- up state (exhibition period)
- Only loud noises wake one up, then confused
- dreams ( nightmares)
REM SLEEP
- EEG desynchronised, high frequency theta and beta activity
- EMG becomes silent -> loss of muscle tone -> paralysed
- Most of spinal -, cranial motor neurons strongly inhibited
- Don’t react to noises but meaningful stimuli such as name
- Brain very active (dreaming)
- Cerebral blood flow and oxygen consumption increase
Activation-synthesis hypothesis
signals supplied to cortex are random and the cortex tries to make sense of it
Sleep cycle
- Each cycle about 90 minutes long
- 20-30 mins of REM-sleep
- Most slow wave sleep in first half then more and more stage 2
- most REM sleep in second half
Adenosin
- control of sleep
- Wakefulness decreases glycogen levels
- > causes an increase in extracellular adenosine levels
- > inhibitory effect on neural activity
- serves as sleep-promoting substance
- Caffeine blocks adenosine receptors
- Less adenosine less SWS
Acetylcholine
= role in arousal
-High ACh levels during waking and REM-sleep, low during SWS
Norepinephrine
- LC (locus coeruleus) neurons increase attention
- Firing high during wakefulness, low during SWS, almost zero during REM
Serotonin (5-HT)
- role in activating behaviour
- Stimulation causes cortical arousal
- Facilitation of continuous automatic movements (chewing, pacing,… )
- Supressing processing of sensory information, precenting reactions that might disrupt ongoing activity
Histamine
= role in arousal
-High during waking, low during sleeping
Orexin/hypocretin
- cell bodies located in lateral hypothalamus
- Most active during active waking, exploratory activity
Recuperation theory
= being awake disrupts homeostasis (internal physiological stability) and sleep is required to restore it
-Restore energy levels or clear toxins
Why?
pro: animals sleep even when it endangers them
adaption theories
= sleep result of internal 24-hour timing mechanism
- Programmed to sleep at night regardless of what happens during the day
- Highly motivated to engage in sleep but don’t need it to stay healthy
niche adaption
=forces individual to conform to a particular ecological niche for which it is well adapted
Memory consolidation
So something about sleep must help brain to retain and form synapses
-Although necessary for survival – not necessarily needed in large quantities
Zeitgeber
daily cycle of light and dark entrains (controls timing of) circadian rhythms
Free-running rhythms
= reticular activating system
- Duration = free running period = relatively constant around 24.2 hrs
- Internal biological clock that is running a little late without external cues
- Support for circadian factors over recuperative factors in regulation of sleep
- Don’t have to be learned
Reticular formation
= reticular activating system
- Wakefulness
- Cycle disrupted when lesion to reticular formation core of brain stem, electrical stimulation awakens
- Low levels of activity: sleep
- High levels of activity: wakefulness
Reticular REM-Sleep nuclei
= REM sleep controlled by nuclei scattered throughout the caudal reticular formation
-REM becomes active when network of independent structures becomes active together
Pons
sends signals that shut off neurons in the spinal cord, causing temporary paralysis of limb muscles
hypothalamus
= switch between REM,NREM and wakefulness
-Hypocretin prevents transition from wakefulness directly into REM
Basal forebrain
- promotes sleep and wakefulness
- release of adenosine from cells in the basal forebrain and other regions supports our sleep drive
SCN ( Suprachiasmatic nucleus)
Clusters of thousands of cells that receive information about light exposure directly from the eyes and control our behavioral / circadian rhythm
pineal gland
It receives signals from the SCN and increases the production of melatonin (helps us sleep)
Insomnia
= difficulty falling asleep (sleep-onset) or staying asleep (sleep-maintenance)
- Sleep-stage misperception: think we weren’t asleep even though we were
- Situational factors like shift work contribute
- Nearly everybody (especially those who snore) have it occasionally but not to the extent that it interferes with sleep
- During an episode: level of CO2 in blood rises and stimulates chemoreceptors -> wake up gasping for air
sleep apnea
unable to sleep and breathe at the same time
Narcolepsy
= sleep attacks
- Enter REM-Sleep right away
- inappropriate activation of the cataplexy pathway normally restricted to REM sleep
- When strong emotional reactions (laughter & anger) sudden physical effort
Cataplexy
varying amounts of muscle weakness up to paralysis while being conscious
Hypnagogic hallucinations
person dreams while lying awake, paralysed
REM behaviour disorder (RBD)
=
acting out of dreams during REM-sleep
- Motor cortex very active but normally motor neurons inhibited
- Damage to nucleus magnocellularis which controls muscle relaxation during REM sleep
REM-Sleep deprivation
- The longer the deprivation the more often initiation of REM sleep (had to be woken up more often)
- Default theory: difficult for brain to stay in NREM sleep so periodically changes to one of the other states
- If immediate bodily needs: switch to wakefulness, if not REM
- REM functions to prepare body for waking
REM rebound
more REM sleep the first few nights after deprivation
Sleep deprivation increases the efficiency of sleep
- deprived have higher proportion of slow wave sleep that seems to serve as main restorative function
- Regain only small proportion of sleep but most of SWS
- Less sleep – same amount of SWS
- Waking up from SWS has major effect on sleepiness the next day
hypnotic drugs like Benzodiazepines
-increase sleep
GABA agonists
Anti-hypnotic drugs
reduce sleep
