aleep and consciousness Flashcards
Function of general sleep
1) RESTORATIVE HYPOTHESIS (REGENERATION)
2) ADAPTIVE REACTION
REGENERATION)
in animal expts: may cause death, loss of weight and body care
after deprivation: SWS4 and REM is made up
effect of physical effort? sleep pattern of patients confined to bed
ADAPTIVE REACTION
avoidance of predators
REM – effect of meaningful stimuli – chance to survive
FUNCTIONS OF REM
developmental hypothesis: newborns of predators (and man) need more
in learning and memory: selective REM deprivation slows down learning, memory functions are impaired
4 phases and REM
o Frequency gets lower, amplitude increases
o Just before sleep still alpha waves, phase 2 sleep spindles, 3 and 4 deep relaxation (slow wave)
o Tonic REM with phasic activity
o 90 minute cycles throughout the night, about 7 hours of sleep, 3-4 REM phases → differs
Neuronal Regulation of Sleep in Wakeefulness → producing area between two levels of transaction (EEG)
o Cerveau isolé → permanent sleep (all raphe are cut from brain)
o Encephale isolé → unchanged sleep pattern (at least some raphe are still at brain)
- ARAS
(Ascending reticular activating system and Raphe system
Neuronal Regulation of Sleep in Activation of specific neural circuits triggers sleep and wakefulness
o Cholinergic neurons of ARAS → awaken
o Slow electrical stimulation of thalamus → fall asleep
o Posterior hypothalamus → arousal (ergotrop)
o Anterior hypothalamus → sleep (trophotrop)
- REM → ACh neurons become active in pons
o Loss of muscle tone
Inhibitory neuron in medulla → to motor neuron and muscle
o Eye movements, PGO waves → Pons → lateral geniculate → occipital cortex
Each wave is synchronized with an eye movement
o Desynchronized EEG
o Hippocampal theta rythm
- Biochemical regulation of SWS
o Glycogen metabolism → adenosine is released (inhibitory neuromodelator) → induces SWS
Caffeine is adenosine inhibitor
o Following sleep deprivation
S-factor (muramil peptides)
DSIP (deep sleep inducing factor)
o Sleep proting substance (SPS, uridin)
o Stimulation of basal forebrain cholinergic system causes ACh increase in cortex and concomitant EEG desynchronization
- Biochemical regulation of REM
o Noradrenergic system → locus coeruleus (medulla)
o Serotinergic system → raphe nuclei
o Both stop during REM, increasing activity of cholinergic system (pons) during REM
- Sleep and thermoregulation
o Part of basal forebrain is center (preoptic part of hypothalamus) of thermoregulation → its warming causes SWS
Warming face or body increases SWS
During SWS brain temperature decreases
During REM temperature of brain increases
Sleep disorders
- Insomnia
- Narcolepsy
Sleep attack
Cataplexy
Sleep paralysis
Hypnagogic hallucinations - Somnambulism
- Narcolepsy
→ disorder of REM
- sleep attack
normal sleep for a few minutes
- cataplexy
loss of muscle tone durink awake state
- Sleep paralysis
before going to sleep or before waking up.
- Hypnagogic hallucinations
frightning
- Somnambulism
combined sleep and wakefulness
Circadian rhythms
Biological clock
- Retinohypothalamic pathway
o Nucleus suprachiasmaticus (in hypothalamus) → pineal glad (melatonin).
- SCN transplanted into other brain causes change of circadian rhythm → the secretion of the hypothalamic hormones is also changed
ATTENTION passive and active
orientating reaction (reflexes) vs selective attention
- Skinner-Yingling model
o Frontal cortex → modality specific inhibition in NR – relevant channel activated o MRF (mesencephalic reticular formation)→ result of inhibition of NR
Consciousness criteria
correct awareness of self and enviroment and space
continuity and clarity
- Disorders of consciousness (organic disorders with known causes)
o Hypnogenic disturbance (somnolentia, spoor, coma); Lesion in ARAS, Disturbed EEG
o Permanent vegetative state (apallic syndrome – cortex) - Cognitive functions are lost, Autonomic functions remain normal, Pathological reflexes, Decorticate muscle tone, Lesion in neocortex
o Akinetic mutism ; Lesion in medial prefrontal lobe or anterior cingular region
o Delirium (hallucinations with normal arousal)
o Confused state (e.g. after epileptic seizure)
o Locked-in syndrome. Conscious but unable to move or to express. Lesion in pons or midbrain
When glutamate is activated channel,
ca and na enter into the neuron → activating pattern
Strong synapse activated whole neuron
o Mechanism of LTP
In resting state magnesium blocks the channel, when activation by glutamate molecule magnesium is pushed away and calcium is allowed to enter
Glutamate binds with NMDA receptor
Depolariszation evicts MG Ion
Amnestia retrogerade
before trauma is lost
