aleep and consciousness Flashcards

1
Q

Function of general sleep

A

1) RESTORATIVE HYPOTHESIS (REGENERATION)

2) ADAPTIVE REACTION

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2
Q

REGENERATION)

A

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

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3
Q

ADAPTIVE REACTION

A

avoidance of predators

REM – effect of meaningful stimuli – chance to survive

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4
Q

FUNCTIONS OF REM

A

developmental hypothesis: newborns of predators (and man) need more
in learning and memory: selective REM deprivation slows down learning, memory functions are impaired

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5
Q

4 phases and REM

A

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

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6
Q

Neuronal Regulation of Sleep in Wakeefulness → producing area between two levels of transaction (EEG)

A

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)

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7
Q
  • ARAS
A

(Ascending reticular activating system and Raphe system

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8
Q

Neuronal Regulation of Sleep in Activation of specific neural circuits triggers sleep and wakefulness

A

o Cholinergic neurons of ARAS → awaken
o Slow electrical stimulation of thalamus → fall asleep
o Posterior hypothalamus → arousal (ergotrop)
o Anterior hypothalamus → sleep (trophotrop)

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9
Q
  • REM → ACh neurons become active in pons
A

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

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10
Q
  • Biochemical regulation of SWS
A

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

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11
Q
  • Biochemical regulation of REM
A

o Noradrenergic system → locus coeruleus (medulla)
o Serotinergic system → raphe nuclei
o Both stop during REM, increasing activity of cholinergic system (pons) during REM

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12
Q
  • Sleep and thermoregulation
A

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

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13
Q

Sleep disorders

A
  • Insomnia
  • Narcolepsy
    Sleep attack
    Cataplexy
    Sleep paralysis
    Hypnagogic hallucinations
  • Somnambulism
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14
Q
  • Narcolepsy
A

→ disorder of REM

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15
Q
  • sleep attack
A

normal sleep for a few minutes

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16
Q
  • cataplexy
A

loss of muscle tone durink awake state

17
Q
  • Sleep paralysis
A

before going to sleep or before waking up.

18
Q
  • Hypnagogic hallucinations
A

frightning

19
Q
  • Somnambulism
A

combined sleep and wakefulness

20
Q

Circadian rhythms

A

Biological clock

21
Q
  • Retinohypothalamic pathway
A

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

22
Q

ATTENTION passive and active

A
orientating reaction (reflexes)
vs selective attention
23
Q
  • Skinner-Yingling model
A
o	Frontal cortex → modality specific inhibition in NR – relevant channel activated
o	MRF (mesencephalic reticular formation)→ result of inhibition of NR
24
Q

Consciousness criteria

A

correct awareness of self and enviroment and space

continuity and clarity

25
Q
  • Disorders of consciousness (organic disorders with known causes)
A

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

26
Q

 When glutamate is activated channel,

A

ca and na enter into the neuron → activating pattern

 Strong synapse activated whole neuron

27
Q

o Mechanism of LTP

A

 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

28
Q

Amnestia retrogerade

A

before trauma is lost