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Physiological Psychology > Chapter Eight > Flashcards

Chapter Eight Flashcards

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1
Q

Electromyogram

A

EMG; records muscle tone

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2
Q

Electro-oculogram

A

EOG; eye movement

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3
Q

Electroencephalogram

A

EEG; electrical activity of brain

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4
Q

How many sleep cycles do you go through in a typical night of sleep?

A

about five

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5
Q

How long does it take to get through one cycle of sleep?

A

about an hour and a half

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6
Q

Stage One of sleep

A

10 minutes; theta waves; easily woken up

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7
Q

Stage Two of sleep

A

K complex; sleep spindles

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8
Q

What are sleep spindles?

A

thought to be a by product of brain that becomes active during stage two of sleep; filters out distractions/noises that wake you up

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9
Q

Stage 3/4 of sleep

A

delta waves; stage four is deepest; “slow wave sleep”; most early in the night

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10
Q

which stages does Non-REM take place?

A

stages 1-4

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11
Q

Does REM get longer with each entry into REM?

A

Yes

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12
Q

What increases during REM?

A

eye movement; the 6 eye muscles are the only muscles that move during REM

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13
Q

What happens to muscle tone during REM?

A

It is lost

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14
Q

What happens to cerebral blood flow during REM?

A

it increases

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15
Q

How much dreaming occurs during REM?

A

about 85% (15% nREM)

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16
Q

Refractory period of REM

A

once awakened, cannot reenter REM for 90 mins; suggests an internal clock regulates this process

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17
Q

Restorative reason for sleep

A

we need sleep to restore us mind and body; mentally and physically

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18
Q

Cognitive reason for sleep

A

we need to sleep in order to form memories; brain needs to be removed from constant stimuli

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19
Q

Evolutionary reason for sleep

A

all humans do this so it must be important. seen as adaptation to benefit survival

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20
Q

Fatal Familial Insomnia

A

genetic; damage to regions in or near the thalamus

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21
Q

What are the symptoms of fatal familial insomnia?

A

insomnia, confusion, loss of autonomic NS

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22
Q

What is the life expectancy for fatal familial insomnia?

A

12 mos. after diagnosis; usually diagnosed in adulthood- mid thirties to forties

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23
Q

What happens to lab animals with lack of sleep?

A

They will die; prior to death they develop other problems

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24
Q

Complete sleep deprivation

A

miss one whole night of sleep

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25
Q

Partial sleep deprivation

A

person sleeps every night but not as much as they should or need

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26
Q

REM deprivation

A

allow a person to sleep except during REM

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27
Q

Slow wave sleep

A

allows brain to rest

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28
Q

REM rebound effect

A

will enter REM more quickly with deprivation; get more REM when deprivation stops

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29
Q

Deprived animal

A

will lose up to 90% of sleep

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30
Q

“Yoked” control animal

A

will lose about 30% of sleep; stays healthy

31
Q

Relationship between exercise and sleep

A

no clear relationship between the two; working certain brain areas “hard” may result in more slow wave sleep in those areas

32
Q

Function of REM sleep

A

critical for brain development; used to consolidate memories; used for learning- if taught task and REM deprived–> learning is slower

33
Q

How much time do newborns spend in REM?

A

disproportionate to adults; 50%

34
Q

Do developed species spend more or less time in REM?

A

more

35
Q

Chemical control of sleep

A

chemicals are involved in sleep, as certain drugs cause drowsiness while others cause sleeplessness; has to be more than chemicals since dolphins can sleep one brain half a time

36
Q

noradrenergic

A

in the locus coeruleus (deep in brain stem) when awake they fire, when asleep they stop

37
Q

acetylcholinergic

A

in pons which produce cortical activity; agonists increase cortical activity, antagonists decrease it

38
Q

serotinergoc

A

in raphe nucleus- fire rapidly when awake, and less rates of firing when asleep

39
Q

histaminergic

A

in hypothalamus that increase cortical arousal; antagonists increase drowsiness.

Benedryl an anti-histamine causes drowsiness

40
Q

Ventrolateral preoptic area (VPL)

A

found in the forebrain, rostral to hypothalamus ; increase in firing due to slow wave sleep

41
Q

What happens to rats with a lesion in their VPL?

A

it produces insomnia and later death within three days

42
Q

Where are the inhibitory GABA connections to in the VPL?

A

raphe nucleus, locus coeruleus, and mammillary nucleus

43
Q

What is REM controlled by?

A

the pons

44
Q

What is REM sleep preceded by?

A

PGO waves (pons, geniculate, and occipital) brief pulses of activity

45
Q

What is the only way PGO waves can be observed?

A

by putting electrodes into the brain

46
Q

What do the PGO waves have to do with our dreams?

A

likely why our dreams are so visual in nature

47
Q

What is the executive mechanism

A

Acetylcholine

48
Q

What do antagonists do to intervals between REM bouts?

A

lengthen them (90 mins)

49
Q

What do agonists do to intervals between REM bouts?

A

shorten them

50
Q

Do levels of Ach increase or decrease during REM?

A

increase

51
Q

Where are the Ach neurons found?

A

peribrachial area

52
Q

What do lesions in the peribrachial area do?

A

reduce REM sleep

53
Q

REM “flip flop”

A

neurons in regions are either ON/OFF and both cannot be active at the same time; switches occur very fast which explains why narcolepsy symptoms occur quickly

54
Q

Insomnia

A

affects 25% occasionally and 10% chronically; symptoms resemble depression;

55
Q

Why are meds prescribed not best option for those with insomnia?

A

tolerance and rebound effect

56
Q

Sleep apnea

A

disturbance of breathing while asleep; may occur hundreds of times per evening

57
Q

Narcolepsy

A

directly fall into REM sleep..will sleep for 2-5 minutes; stimulant meds and frequent napping

58
Q

Cataplexy

A

awake, but complete loss of muscle tone; triggered by excitement; a couple minutes like narcolepsy and then back to normal

59
Q

Sleep paralysis

A

a symptom of narcolepsy- paralysis creeps into waking

60
Q

hypnagogic hallucinations

A

another symptom of narcolepsy-dream like states invade waking

61
Q

REM without atonia

A

loss of muscle tone does not occur during REM-flip flop does not occur; physically and behaviorally act out dreams

62
Q

What do meds used to treat cataplexy do to those with REM without atonia?

A

make them worse

63
Q

REM sleep disorders

A

narcolepsy, cataplexy, REM without atonia, sleep paralysis, and hypnagogic hallucinations

64
Q

Biological clocks

A

predictable changes in physiological function occur in different time intervals (rhythms)

65
Q

Zeitgebers

A

time giver; synchronize circadian (daily) rhythms

66
Q

What is zeitgeber for regulating sleep?

A

natural light

67
Q

Where is the sprachiasmatic nucleus found?

A

found in the hypothalamus

68
Q

What happens when suprachiasmatic nucleus is lesioned?

A

many rhythms are disrupted: sleep, wheel running, hormone secretions

rats with this lesion do not show normal sleeping patterns- they sleep sporadically but get the same amount

69
Q

Where do the projections from the SCN come from?

A

the retina

70
Q

What happens when you transplant a SCN?

A

restoration of the disrupted rhythms

71
Q

Silver et al. research

A

transplanted SCN tissue in a semi permeable capsule and it restored the rhythms

72
Q

Does SCN lesions disrupt breeding cycles?

A

Yes, which are activated with “day length” in spring

73
Q

What do SCN lesioned males do differently?

A

secrete testosterone year round, as opposed to “peaks” during breeding season

74
Q

Is the pineal gland important to the SCN?

A

yes, it receives input from the SCN.

melatonin is secreted by pineal, which changes as seasons change (and light exposure changes)

Physiological Psychology (11 decks)

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