Chapter 19: Brain Rhythms and Sleep Flashcards

1
Q

(): changes in physiological functions
according to brain clock

A

Circadian rhythms

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2
Q
  • measurement of generalized activity in the cerebral cortex
  • helps diagnose neurological conditions (e.g. epilepsy, sleeping disorders) ++ research
A

electroencephalogram (EEG)

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3
Q

amplitude of EEG signal = measure of () of underlying neurons (particularly dendrite excitation)

A

synchronous activity

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4
Q

Recording of miniscule magnetic signals generated by neural activity (one billionth of the magnetic field generated by the Earth, power lines, etc.)

A

magnetoencephalography (MEG)

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5
Q

compare MEG, EEG, fMRI, PET

A
  • MEG has better localization of neural activity vs EEG
  • MEG has low (or no) spatial resolution (images); c.f. fMRI and PET
  • EEG + MEG = fast neuron activity
  • fMRI + PET = changes in blood flow or metabolism
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6
Q

EEG rhythms often correlate with particular states of ()

A

behavior

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7
Q

categorization of EEG rhythms is primarily based on ()

A

frequency

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8
Q

EEG Rhythms

(low, high) synchrony, (low, high) amplitude: alertness and waking OR dream state of sleep

A

low synchrony, low amplitude

neurons aren’t in sync -> involved in diff aspects of cognitive task

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9
Q

(low, high) synchrony, (low, high) amplitude: deep, non-dreaming sleep OR coma/drugged states

A

high synchrony, high amplitude

neurons aren’t engaged in info processing

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10
Q

2 ways that rhythms can be set in neuronal activity

A
  1. neurons may take cues from a central clock (pacemaker)
  2. neurons share or distribute the timing function via mutual inhibition or activation

in mammalian brain, both methods coordinate synchronous activity

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11
Q

() can serve as massive cortical input as a pacemaker

A

thalamus

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12
Q

hypothesis on brain rhythm function

sleep rhythms as the brain’s way of ()

A

disconnecting cortex from sensory input

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13
Q

hypothesis on brain rhythm function

walter freeman: () coordinate activity of nervous system regions

A

neural rhythms

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14
Q

() seizure: entire cerebral cortex, complete behavior disruption, consciousness loss

A

generalized

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15
Q

tonic-clonic seizure: () driven by tonic (ongoing) or clonic (rhythmic) patterns

A

muscle groups

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16
Q

() seizure: < 30 seconds of generalized 3 Hz EEG waves with subtle motor signs

A

absence

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17
Q

() seizure: circumscribed cortex area, abnormal sensation or aura

A

partial

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18
Q

partial seizures in the temporal lobe result in:

A

deja vu, hallucinations

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19
Q

readily reversible state of reduced responsiveness to, and interation with, the environment

A

sleep

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20
Q

() sleep: EEG similar to awake state, only eye nd respiratory muscles move, vivid dreams, high O2 consumption, active sympathetic division

A

rapid eye movement (REM)

an active, hallucinating brain in a paralyzed body

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21
Q

() sleep: slow, large amplitude EEG -> sensory inputs can’t reach cortex, low movement and muscle tension, active parasympathetic NS, low body temp and energy consumption

A

non-REM (slow wave)

an idling brain in a movable body

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22
Q

body during REM sleep

():body paralzyed except eye and respiratory muscles

A

REM atonia

almost complete loss of skeletal muscle tone

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23
Q

describe the 4 stages in a sleep cycle

A

stage 1: transitional sleep
stage 2: slightly deeer sleep (thalamus-driven sleep spindles)
stages 3-4: deep sleep (slow, low-amplitude)

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24
Q

compare the first sleep cylce to the later sleep cycles when sleeping

A

first cycle: stage 1: a few min; stages 2-3: 5-20 min each; stage 4: 20-40 min

later cycles: REM sleep duration increases; non-REM sleep (esp stages 3-4) decreases.

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25
Q

What is the proper length of sleep? – ()

A

whatever amount that allows you maintain a reasonable level of alertness during the day

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26
Q

Early teenagers (high school students) have a similar demand for sleep as preadolescents, but fall asleep late due to changes in (1); yet, earlier start of the school day causes (2)

A
  1. circadian timing mechanisms
  2. chronic sleep deprivation
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27
Q

All mammals, birds, and reptiles appear to sleep, although only mammals and some birds have a () phase

A

REM

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28
Q

Sleep mainly for the (1); Sleep deprivation -> (2)

A
  1. brain
  2. cognitive impairment
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29
Q

explain sleep in the bottlenose dolphin

A

~2 h of non-REM sleep on just one side, then 1 h awake on both sides, 2 h of non-REM sleep on the other side, and so on (total 12 h per night)

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30
Q

Two main categories of theories of sleep function

A
  1. restoration - sleep to rest and recover
  2. adaptation - avoid trouble, conserve energy
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31
Q

restoration during sleep

  1. () - cells repair and regrow; no sleep -> loss of immune function
  2. () - glymphatic (waste clearance) system clears out toxic byproducts; plasticity
A
  1. cellular restoration
  2. brain functions
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32
Q

REM sleep deprivation causes () even though REM deprivation does not cause major harm during the day time

A

REM rebound - sending more time in REM sleep when left to sleep undisturbed

33
Q

dream function accdg to Freud

dream function -> disguised (): unconscious way to express sexual and aggressive fantasies

A

wish fulfillment

34
Q

dreams accdg to Hobson and McCarley

(): Pons, via thalamus, activates various areas of the cortex, and the cortex tries to synthesize the disparate images into a sensible whole

explains weirdness, but not recurring dreams

A

activation-synthesis hypothesis

35
Q

relationship beteween sleep and memory

A
  • intense learning increases REM sleep duration
  • REM deprivation prevents performance improvement
36
Q

Sleep-wake cycle continues without sensory inputs -> Sleep is an ()

A

active process

37
Q

() may induce prolonged sleep or prolonged wakefulness

A

Brainstem lesions

38
Q

Critical neurons for control of sleep-wake cycle are part of the () systems

A

diffuse modulatory neurotransmitter

39
Q

Critical neurons for control of sleep-wake cycle

() neurons: enhance and fire during waking state

A

NE, 5-HT

40
Q

Critical neurons for control of sleep-wake cycle

() neurons: some enhance REM events, others are active during waking state

A

cholinergic

41
Q

elaborate on how diffuse modultory systems can block sensory input to cortex

A

DMS can control rhythmic behavior of thalamus -> thalamus acts as pacemaker and influences cortical EEG; sleep rhythms of thalamus block sensory input

42
Q

sleep also involves activity in () (e.g., inhibition of motor neurons during dreaming)

A

descending branches of diffuse modulatory systems

43
Q

Moruzzi’s research

relationship of brain stem and sleep

A
  1. lesions in midline of brain stem -> state similar to non-REM sleep
  2. electrical stim of midline tegmentum (midbrain) changes cortical EEG from slow, rhythmic (non-REM) to alert and aroused state
44
Q

Moruzzi’s research

if this region is stimulated, cortical EEG from slow, rhythmic (non-REM) to alert and aroused state

A

ascending reticular activating system

45
Q

Neurons that increase firing rates in anticipation of awakening and during arousal: (5) -> synapse directly on the entire thalamus, cerebral cortex, and many other brain regions

General effects: depolarization, excitability, and suppression of rhythmic firing

A
  1. NE (locus coeruleus)
  2. 5- HT (raphe N)
  3. ACh (brain stem & basal forebrain)
  4. histamine (midbrain)
  5. hypocretin (hypothalamus) neurons
46
Q

loss of hypocretin neurons leads to sleep disorder:

A

narcolepsy

47
Q

stages of non-REM sleep

A
  1. EEG sleep spindles
  2. spindles disappear
  3. slow, delta rhythms
48
Q

role of thalamic neurons in non-REM sleep

A
  • sleep spindles generated by inherent rhythmicity of thalamic neurons
  • delta rhythms occur when thalamic neuron MP becomes much more negative than during sleep spindles
49
Q

synchronization of activity during spindle or delta rhythms is due to () within the thalamus and between the thalamus and cortex

A

neural interconnections

50
Q

REM sleep: PET Images

3 main things in PET images during REM sleep

A
  1. highly active extrastriate cortex
  2. high limbic activation
  3. low frontal activity
51
Q

REM sleep: PET images

high activity of extastriate cortex thought to be (internally/externally) generated

A

internally

52
Q

emotional components of dreams thought to be caused by ()

A

high limbic activation

53
Q

low frontal activity during REM sleep implies:

A

no high-level integration or interpretation of info from extrastriate cortex

buzz of uninterpreted visual imagery

54
Q

control of REM sleep by brain stem neurons

  1. LC and raphe N: activity (increases/decreases)
  2. Pons cholinergi neurons (increases/decreases)
A
  1. decreases
  2. increases
55
Q

brain stem neuron activity during REm sleep also inhibits ()

A

spinal motor neurons

56
Q

() arises from the disruption of the bain stem systems that normally mediate REM atonia

A

REM sleep behavior disorder

act out (i.e. move their bodies) during REM accdg to some dreams

57
Q

sleep promoting factors

() - released by neurons (gradual increase during waking period); may have inhibitory effects on diffuse modulatory systems

A

adenosine

58
Q

sleep promoting factors

(): increased during waking; abundant in wake- promoting ACh neurons; triggers release of adenosine

A

Nitric acid (NO)

59
Q

sleep promoting factors

(): produced by bacteria; facilitates non-REM sleep

A

Muramyl dipeptide

60
Q

sleep promoting factors

(): synthesized in brain, stimulates immune system, induces fatigue and sleepiness

A

Interleukin-1

61
Q

sleep promoting factors

(): released at night, inhibited during daylight; helps initiate and maintain sleep—used to treat symptoms of jet lag and insomnia

A

Melatonin

62
Q

Gene expression during sleep and waking

0.5% of genes showed differences of expression levels when awake or asleep.
– Genes that increased in awake rats: (1)
– Genes that increased in sleeping rats: genes that contribute to ()

A
  1. immediate early genes, mitochondrial genes & cellular stress genes
  2. protein synthesis and plasticity mechanisms

these changes are specific to brain

63
Q

Narcolepsy involves direct transition from ()

A

waking state to REM sleep

64
Q

narcolepsy symptoms

excessive daytime sleepiness

A

sleep attack

65
Q

narcolepsy symptoms

waking to REM atonia with consciousness; often caused by strong emotions

A

cataplexy

66
Q

group of unusual behaviors before falling asleep, during sleep, or in the time between sleep and wakefulness

A

parasomnia

e.g. dream enactment (REM behavior disorder), sleep walking, bed-wetting, sleep paralysis

67
Q
  • daily cycles of light and dark -> but behaviors continue even if daylight and darkness cycles are removed
  • behavior of most animals is coordinated to cycle
A

circadian rhythms

68
Q

collective term for environmental time cues

A

zeitgebers

69
Q

(): Mammals completely deprived of zeitgebers settle into rhythm of activity and rest but drift out of phase with 12-hour day/light cycle

A

Free-run

70
Q

primary zeitgeber for mature mammals

A

light-dark cycle

71
Q

() of SCN -> shift of circadian rhythm in a predictable way

A

Electrical stimulation

72
Q

() of SCN -> abolishes circadian rhythmicity of physical activity, sleeping and waking, and feeding and drinking

A

Bilateral removal

73
Q

() to SCN necessary to entrain sleep cycles to night

A

Retinal input

74
Q

specialized photopigment of photoreceptor that synapses directly onto SCN neurons to reset circadian clock (light-sensitive ganglion cells)

A

melanopsin

75
Q

other term for light-sensitive ganglion cells

A

intrinsically photosensitive retinal ganglion cells

75
Q

SCN output axons to parts of the hypothalamus, midbrain, diencephalons; use (1) as primary neurotransmitter; SCN neurons may also release () rhythmically

A
  1. GABA
  2. vasopressin
76
Q

clock that functions even without APs -> molecular cycle based on ()

A

gene expression (of clock genes)

77
Q

examples of clock genes

A

period (per), cryptochrome, clock