Chapter 9 - Sleep Flashcards
daily rhythmical change in behaviour or psychological process
circadian rhythms
stimulus that resets the biological clock responsible for circadian rhythms
zeitgebers
SCN
central to biological clocks
- a hypothalamc nucleus containing the biological clock for many of the body’s circadian rhythms
- lesions disrupt circardian rhymths of wheel runing etc.
- provides primary control over the timing of sleep cycles.
retinohypothalamic pathway
direct projection from retina to SCN
photochemical
melanopsin (ganglion cells)
how does SCN control sleep/wake cycle
SPZ - DMHz - vlPOA & orexin in LH
projections to vlPOA are
inhibitory - inhibit sleep
projections to orexin neurons in LH are
excititory - promote wakefulness
measure neural events
EEG
measure eye movements
EOG
measure muscle tension
EMG
large disk electrode places on scale record electrical potentials
- extracellular voltage changes over large area of cortex
EEG
stages of sleep
alert - low amplitude, high freq. beta waves
drowsy - similar to alert but, occasional alpha waves
stage 1 - similar to alert but, slower and higer amplutide (theta waves)
stage 2 - similar to stage 1 bur, ossasional sleep spindles and K-complexes
stage 3 - slower, larger, occasional delta spikes
stage 4 - predominance of delta spikes
low amplitude, high frequency. beta waves
alert
low amplitude (slightly higher), occasional alpha waves
drowsy
slower and higher amplitude. theta waves
- light sleep, muscle activity slows down, occasional muscle twitching
stage 1
occasional splindles and k-complexes. (large negative followed by large positive deflection)
- breathing pattern and heart rate slows. slight decrease in body temperature.
stage 2
slower, larger , occasional delta spikes
- deep sleep begins. brain begins to generate slow delta waves
stage 3
predominance of delta spikes
- very deep sleep. rhymthic breathing. limited muscle activity. brain produces delta waves.
stage 4
loss core muscle tone
low amplitude, high frequency EEG
cerebral activity (O2 consumption, blood flow, neural firing) increases to waking levels
general increase in NS (bp, pulse)
when awaken, person appears alert and attentive
- penile erection/vaginal secretion
- dreams
- EEG desynchrony (rapid, irregular waves)
REM
EEG synchrony (slow waves)
moderate muscle tone
slow or absent eye movement
lack of genital activity
SWS
dreams during non-rem sleep
isolated experiences (ie: free falling)
dreams during rem sleep
stories
disguised versions of our real dreams
information that the conscious individual remembers experiencing. It consists of all the elements of actual images, thoughts, and content within the dream that the individual is cognitively aware of upon awakening.
manifest dreams
illustrates the hidden meaning of one’s unconscious thoughts, drives, and desires
latent dreams
information supplied to the cortex during REM sleep is largely random and that the resulting dream is the cortex’s effort to make sense of these random signals
activation-synthesis theory
REM
high blood flow to visual association cortex
low in primary visual cortex and PFC
- low activity in primary visual cortex - no input to eyes
- high level in visual association cortex - visual hallucinations that occur during day dreaming
- low in PFC - dreams are poorly organized with respect to time and other PFC tasks
nightmares
SWS - stage 4.
sleep restriction therapy
- the amount of time that an insomnia is allowed to spend in bed is reduced
- after a period of sleep restriction, the amount of time spend in bed is gradually increased in small increments
medical causes of insomnia
sleep apnea
periodic limb movement disorder
restless leg syndrome
fall asleep and then cease to breath
- CO2 in blood stimulates chemoreceptors, and person wakes up, grasping for air, O2 levels return to normal, person goes back to sleep, cycle begins again
sleep apnea
obstruction of the respiratory passages by muscle spasms or atonia (lack of muscle tone)
obstructive sleep apnea
failure of CNS to stimulate respiration
central sleep apnea
periodic, involuntary movements of the limbs
- twiched of legs during sleep
- often unaware
periodic limb movement disorder
complain of hard-to-describe tension of uneasiness in legs that prevents sleeping
restless leg syndome
treatment for periodic limb movement disorder and restless leg syndrome
DA agonists
hypersomnia
narcolepsy
dream while awake
hypnogogic hallucinations
severe daytime sleepiness
boring conditions
narcoleptic sleep attacks
just before wake or sleep
sleep paralysis
sudden loss of muscle tone - emotional conditions - remains conscious
cataplexy
difficulty staying awake
REM sleep intrudes into waking state
- skip sws - go directly to REM from waking
sleep is fragmented - disrupted by periods of waking
- heredity disorder - gene on chromosome 6 strongly influenced by unknown environmental factors
narcolepsy
simulant treatment for narcolepsy
methylphenidate (ritalin)
treatment for cataplexy, sleep paralysis, hypnagogic hallucionations
antidepressants
newly avalible stimulant for narcolepsy that acts on orexinergic neurons.
increase Fos protein in orexin neurons
modafil
some people with this disorder act out their dreams
- rare, almost opposite of cataplexy
- caused by lack of inhibtion of motor neurons that normally occurs during REM sleep
REM sleep behaviour disorder
structure of the caudal RF that controls muscle tone during REM sleep
nucleus magnocellularis
bedwetting
nocturnal enuresis
sleep walking
somnambulism
night terror
pavor nocturnus
eating during sleep walking, often without recollection
sleep-related eating disorder
deficits in attention and memory
dreamlike, confused state, loss of control of ANS, insomnia, fatal.
fatal familial insomnia
related to mad cow disease
REM sleep faciliates the consolidation of ___
nondeclarative memory
SWS facilitates the consolidation of ______
declarative memory
conscious recollection of facts and events (semantic and episodic memory)
declarative/explicit
experience can alter behaviour without us being consciously aware of exactly what we have learned
nondeclarative/implicit
nucleoside whose primary role in the control of sleep
adenosine
role of adenosine in sleep
- astrocytes - stock glygogen
- increase in brain activity, glycogen converts to fuel for neurons
- prolonged wakefulness, decrease glycogen in brain
- decrease glycogen, increase adenosine
- inhibit neural activity
- accumilation adenosine - promote sleep
5 NT play role in alertness and wakefulness
ACh NA 5-HT Histamine Orexin
3 groups ACh neurons
Pons Basal forebrain (both activation and cortical desynchrony) medial septum (controls activity of hippocampus)
role ACh
ACh agonists increase EEG signs of cortical arousal
ACh antagonists decrease them
- high levels of SCH in hippocampus and neocortex during REM and waking, low during SWS
role NE in alertness
locus coerules - located in dorsal pons
- release NE through axonal varicosties
- related to behavioral arousal
- firing rate was high during wakefulness, low during SWS, almost zero during REM
- within a few seconds of awakening, firing rate increased dramatically
- increased vigilance: ability to pay attention to stimuli in the environment
beadlike swellings of the axonal branches, contains synaptic vesicles and releases NE
axonal varicosties
ability to pay attention to stimuli in the environment
increased vigilance
role 5-HT
- stimulation of RN causes locomotion and cortical arousal
- PCPA (antagonist) - reduces cortical arousal
- neurons most active during waking
- firing rate decline during SWS
- zero during REM
- facilitate continuous automatic movements
Histamine
- cell bodies located in the TMN of the hypothalamus
- connections to cortex - increase cortical activation and arousal
- activity of histamine neurons is high during waking, low during SWS and REM
- histamine antagonists decrease waking, increase sleep
- antihistamines
orexin
cell bodies located in LH
excititory
Orexin neurons fired at a high rate during alert or active waking and at a low rate during quiet waking, SWS and REM sleep
Preoptic Area
POA
- control of sleep
- contains neurons whose axons inhibit arousal neurons
- destruction of POA produced total insomnia in rats
- stimulation produced signs of drowsiness, sleep
- POA neurons receive inhibitory input histamine, 5-HT, NE neurons
vlPOA
damage supresses sleep, increased Fos during sleep
MnPN
release GABA
- sends axons to orexin, ACh, NE, 5-HT
region of the dorsal pons containing REM-ON cells
SLD
region of the dorsal midbrain containing REM-OFF cells
vlPAG
regions of REM-ON and REM-OFF cells are connected by
inhibitory GABAergic neurons
neurons responsible for muscular paralyisis located just ventral to
REM ON region (SLD)
neurons in SLD send axons to
thalamus (control of cortical arousal)
glutamatergic neurons in medial pons RF - ACh neurons of basal formation (arousal and cortical desynchrony)
ACh neurons to tectum
- rapid eye movement
SCN - day cycle
during the day cycle, DMH inhibits the vlPOA and excites the brain stem and forebrain arousal systems, stimulating arousal
control of seasonal rhythms
pineal gland and melatonin
gland attached to the dorsal tectum; produces melatonin and plays a role in circadian and seasonal rhythms
pineal gland
