Chapter 9 - Sleep Flashcards

1
Q

daily rhythmical change in behaviour or psychological process

A

circadian rhythms

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2
Q

stimulus that resets the biological clock responsible for circadian rhythms

A

zeitgebers

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3
Q

SCN

A

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.
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4
Q

retinohypothalamic pathway

A

direct projection from retina to SCN

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5
Q

photochemical

A

melanopsin (ganglion cells)

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6
Q

how does SCN control sleep/wake cycle

A

SPZ - DMHz - vlPOA & orexin in LH

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7
Q

projections to vlPOA are

A

inhibitory - inhibit sleep

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8
Q

projections to orexin neurons in LH are

A

excititory - promote wakefulness

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9
Q

measure neural events

A

EEG

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10
Q

measure eye movements

A

EOG

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11
Q

measure muscle tension

A

EMG

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12
Q

large disk electrode places on scale record electrical potentials
- extracellular voltage changes over large area of cortex

A

EEG

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13
Q

stages of sleep

A

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

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14
Q

low amplitude, high frequency. beta waves

A

alert

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15
Q

low amplitude (slightly higher), occasional alpha waves

A

drowsy

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16
Q

slower and higher amplitude. theta waves

- light sleep, muscle activity slows down, occasional muscle twitching

A

stage 1

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17
Q

occasional splindles and k-complexes. (large negative followed by large positive deflection)
- breathing pattern and heart rate slows. slight decrease in body temperature.

A

stage 2

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18
Q

slower, larger , occasional delta spikes

- deep sleep begins. brain begins to generate slow delta waves

A

stage 3

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19
Q

predominance of delta spikes

- very deep sleep. rhymthic breathing. limited muscle activity. brain produces delta waves.

A

stage 4

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20
Q

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)

A

REM

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21
Q

EEG synchrony (slow waves)
moderate muscle tone
slow or absent eye movement
lack of genital activity

A

SWS

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22
Q

dreams during non-rem sleep

A

isolated experiences (ie: free falling)

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23
Q

dreams during rem sleep

A

stories

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24
Q

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.

A

manifest dreams

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25
Q

illustrates the hidden meaning of one’s unconscious thoughts, drives, and desires

A

latent dreams

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26
Q

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

A

activation-synthesis theory

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27
Q

REM

A

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

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28
Q

nightmares

A

SWS - stage 4.

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29
Q

sleep restriction therapy

A
  • 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
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30
Q

medical causes of insomnia

A

sleep apnea
periodic limb movement disorder
restless leg syndrome

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31
Q

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

A

sleep apnea

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32
Q

obstruction of the respiratory passages by muscle spasms or atonia (lack of muscle tone)

A

obstructive sleep apnea

33
Q

failure of CNS to stimulate respiration

A

central sleep apnea

34
Q

periodic, involuntary movements of the limbs

  • twiched of legs during sleep
  • often unaware
A

periodic limb movement disorder

35
Q

complain of hard-to-describe tension of uneasiness in legs that prevents sleeping

A

restless leg syndome

36
Q

treatment for periodic limb movement disorder and restless leg syndrome

A

DA agonists

37
Q

hypersomnia

A

narcolepsy

38
Q

dream while awake

A

hypnogogic hallucinations

39
Q

severe daytime sleepiness

boring conditions

A

narcoleptic sleep attacks

40
Q

just before wake or sleep

A

sleep paralysis

41
Q

sudden loss of muscle tone - emotional conditions - remains conscious

A

cataplexy

42
Q

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

A

narcolepsy

43
Q

simulant treatment for narcolepsy

A

methylphenidate (ritalin)

44
Q

treatment for cataplexy, sleep paralysis, hypnagogic hallucionations

A

antidepressants

45
Q

newly avalible stimulant for narcolepsy that acts on orexinergic neurons.
increase Fos protein in orexin neurons

A

modafil

46
Q

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
A

REM sleep behaviour disorder

47
Q

structure of the caudal RF that controls muscle tone during REM sleep

A

nucleus magnocellularis

48
Q

bedwetting

A

nocturnal enuresis

49
Q

sleep walking

A

somnambulism

50
Q

night terror

A

pavor nocturnus

51
Q

eating during sleep walking, often without recollection

A

sleep-related eating disorder

52
Q

deficits in attention and memory

dreamlike, confused state, loss of control of ANS, insomnia, fatal.

A

fatal familial insomnia

related to mad cow disease

53
Q

REM sleep faciliates the consolidation of ___

A

nondeclarative memory

54
Q

SWS facilitates the consolidation of ______

A

declarative memory

55
Q

conscious recollection of facts and events (semantic and episodic memory)

A

declarative/explicit

56
Q

experience can alter behaviour without us being consciously aware of exactly what we have learned

A

nondeclarative/implicit

57
Q

nucleoside whose primary role in the control of sleep

A

adenosine

58
Q

role of adenosine in sleep

A
  • 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
59
Q

5 NT play role in alertness and wakefulness

A
ACh
NA
5-HT
Histamine 
Orexin
60
Q

3 groups ACh neurons

A
Pons 
Basal forebrain (both activation and cortical desynchrony)
medial septum (controls activity of hippocampus)
61
Q

role ACh

A

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

62
Q

role NE in alertness

A

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
63
Q

beadlike swellings of the axonal branches, contains synaptic vesicles and releases NE

A

axonal varicosties

64
Q

ability to pay attention to stimuli in the environment

A

increased vigilance

65
Q

role 5-HT

A
  • 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
66
Q

Histamine

A
  • 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
67
Q

orexin

A

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

68
Q

Preoptic Area

A

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
69
Q

vlPOA

A

damage supresses sleep, increased Fos during sleep

70
Q

MnPN

A

release GABA

- sends axons to orexin, ACh, NE, 5-HT

71
Q

region of the dorsal pons containing REM-ON cells

A

SLD

72
Q

region of the dorsal midbrain containing REM-OFF cells

A

vlPAG

73
Q

regions of REM-ON and REM-OFF cells are connected by

A

inhibitory GABAergic neurons

74
Q

neurons responsible for muscular paralyisis located just ventral to

A

REM ON region (SLD)

75
Q

neurons in SLD send axons to

A

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

76
Q

SCN - day cycle

A

during the day cycle, DMH inhibits the vlPOA and excites the brain stem and forebrain arousal systems, stimulating arousal

77
Q

control of seasonal rhythms

A

pineal gland and melatonin

78
Q

gland attached to the dorsal tectum; produces melatonin and plays a role in circadian and seasonal rhythms

A

pineal gland