Sleep, dreams and consciousness Flashcards

1
Q

How does an EEG machine work

A

Electrodes are placed on the scalp and pick up the electric fields generated by neurons
Small voltage fluctuations are measured between selected pairs of electrodes

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2
Q

EEG activity when awake and attentive

A

Desynchronised, low-voltage high-frequency activity

Gamma and beta rhythms

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3
Q

EEG activity when drowsy or eyes closed

A

Slowed activity, alpha waves appears at 8-12Hz

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4
Q

EEG activity during stage 1 sleep

A

Theta waves (4-8Hz) and amplitude increases slightly

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5
Q

EEG activity during stage 2 sleep

A

Very sharp high-amplitude waves called K complexes, spindles (8-14Hz) in brief epochs involving synchronised thalamocortical activity

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6
Q

Definition of sleep

A

A condition that typically occurs for several hours every day, characterised by immobility, reduced response to sensory stimuli, rapidly reversible

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7
Q

EEG activity during stage 3 and 4 (deep sleep)

A

Continuous delta waves (<4Hz)

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8
Q

EEG activity during REM sleep

A

Similar to awake stage- low voltage, high frequency

Beta and gamma waves

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9
Q

How many times do we cycle through all the sleep stages per night

A

6 times a night

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10
Q

How do we cycle through the different stages of sleep in a night

A

Awake -> NREM stages 1-4->NREM stages 4-1 -> REM sleep ->NREM stages 1-4
Each cycle, deep stage sleep is reduced and REM sleep is prolonged

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11
Q

EOG (electrooculogram) recordings at different sleep stages

A

Awake- rapid eye movement
NREM- slow random eye movements
REM- rapid eye movements

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12
Q

EMG (electromyography) recordings at different sleep stages

A

Awake- continuous, voluntary
NREM- some episodic involuntary movement
REM- motor output commanded but inhibited (due to atonia)

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13
Q

What happens to a mouse if you keep it in complete darkness

A

Circadian rhythm maintained but the mice gradually wake up earlier and earlier, because the mouse’s internal clock is slightly shorter than 24 hours

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14
Q

What is the master pacemaker of circadian rhythms

A

Suprachiasmatic nucleus

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15
Q

What is the result if the suprachiasmiatic nucleus is removed

A

Circadian rhythms break down, animals show random bouts of activity and sleeping

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16
Q

What happens if an SCN neuron is removed and cultured so they have no input

A

The neuron’s gene expression patterns continue to oscillate with the circadian rhythm, but this gradually disappears

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17
Q

What is it called the SCN uses retinal input to synchronise the internal circadian rhythm with light-dark rhythms

A

Photopic entrainment of circadian rhythms

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18
Q

What retinal cells supply the SCN with light-dark info

A

RGCs

Photosensitive RGCs with melanopsin, project directly to the SCN

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19
Q

What determines phase phenomenon in SCN transplants

A

The donor animal’s circadian rhythms

eg transplanting a mouse SCN into a human would shift the human’s circadian rhythm to below 24 hours

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20
Q

Match height of brainstem lesions to their effect

A

Lesions below the pons- normal sleep/wake pattern
Mid-pons lesions- continuously awake
Lesions above the pons- permanently asleep

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21
Q

Why does lesioning different heights of the brainstem cause different wake/sleep disruptions

A

Different brainstem nuclei act as diffuse modulatory systems, regulating global activity

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22
Q

How does the activity of neurotransmitter released by brainstem nuclei differ across wake/sleep

A

ACh, serotonin, DA and NA are all most active during wake and less active during NREM sleep
ACh and DA are active during REM sleep

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23
Q

What is sleep homeostasis

A

If we don’t sleep for a while, sleep pressure builds up

If we don’t sleep for a LONG time, additional sleep pressure builds, and we sleep longer to compensate

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24
Q

Effects of sleep deprivation in humans- all nighter

A

Fatigue, irritability, impaired memory

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25
Q

Effects of sleep deprivation in humans- world record attempts

A

Hallucinations, tremor

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26
Q

Effects of sleep deprivation in humans- chronic

A

Mental health declines, gastrointestinal disorders, increased cancer risk, cardiovascular disorders, all circadian rhythms disrupted

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27
Q

Suggested functions of REM sleep

A

Memory consolidation and transfer, unlearning ‘parasitic’ memory traces, reinforcement of innate behaviours

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28
Q

What does an EEG record look like

A

A set of simltaneous squiggles, indicating voltage changes betweens pairs of electrodes

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29
Q

What does EEG measure

A

The summed voltages generated by the currents that flow during synaptic expectation of the many pyramidal neurons in the cerebral cortex

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30
Q

What detemines the amplitude of EEG

A

How synchronous the activity of underlying neurons is- simultaneous neuron firing sums their tiny signals to create a larger amplitude signal

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31
Q

What is MEG

A

Magnetoencephalography- detecting the magnetic signals produced when neurons generate currents

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32
Q

What are gamma rhythms

A

Fast, 30-90Hz, signal an activated or attentive cortex

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33
Q

What are rippled

A

Brief bouts of 80-200Hz oscillations

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34
Q

What are beta rhythms

A

Relatively fast, 15-30Hz

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35
Q

Why is cortex firing unsynchronised during active waking

A

Each cortical neuron is very active, processing a different aspect of a complex task

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36
Q

What acts as a pacemaker for synchronous neuronal oscillation

A

The thalamus- has huge cortical input

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37
Q

How does the thalamus produce an oscillatory rhythm

A

Thalamic neurons can generate very rhythmic APs- some have a particular set of voltage-gated ion channels for this

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38
Q

How do thalamus oscillations act as a pacemaker for neuronal oscillation

A

The rhythmic activity of thalamic pacemaker neurons are synchronised with one another, then passed to the cortex by thalamocortical axons

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39
Q

A proposed function of synchronised neuronal oscillation

A

Momentary synchronisation of different brain area firing may allow binding of various neural components into a single perceptual construction eg shape/colour

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40
Q

What state is the ANS in in NREM vs REM sleep

A

NREM-> parasympathetic nervous system activated, temp and energy consumption lowered
REM->sympathetic activity, heart and respiration rates increase and become irregular

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41
Q

What is brain activity like during NREM sleep

A

Energy use rate, and general firing rate, are at their lowest point of the day- mental processes are minimal

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42
Q

What is oxygen use like in REM sleep

A

Oxygen consumption is higher than when the brain is awake and doing difficult maths problems

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43
Q

What fractino of sleep is spent in nonREM

A

75%

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44
Q

How is nonREM sleep divided

A

4 distinct stages

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45
Q

NREM stage 1

A

Transitional sleep (lightest stage), slow rolling eye movements, lasts a few mins

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46
Q

NREM stage 2

A

Lasts 5-15 mins, slightly deeper than stage 1, eye movements almost cease

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47
Q

NREM stage 3

A

Slow high-amplitude delta rhythms, eye movements almost cease

48
Q

NREM stage 4

A

Deepest stage, delta rhythms of 2Hz or less, may last 20-40 mins in first sleep cycle

49
Q

What obligatory refractory period exists in sleep cycles

A

Period of about 30mins between periods of REM

50
Q

What are ultradian rhythms

A

Recurrent cycles repeated throughout a 24 hour day

eg sleep cycles

51
Q

How do bottlenose dolphins sleep

A

1 hemisphere at a time- 2 hours of NREM sleep on one side, then 1 hour awake on both sides, then switch hemisphere

52
Q

Effect of sleep deprivation in rats

A

Rats progressively lose weight while consuming much more food, become weak, accumulate stomach ulcers and die- seem to lose ability to regulate body temp and metabolic needs

53
Q

What happens if people are repeatedly deprived of REM sleep by waking them up as they enter it

A

Sleepers attempt to enter REM sleep much mroe frequently than normal
Experience REM rebound when they are allowed to sleep undisturbed, proportional to the duration of their deprivation

54
Q

What is the activation synthesis hypothesis of sleep

A

Random pons charge activates random areas of the cerebral cortex, eliciting associations and memories that are synthesized into dreams

55
Q

What studies suggest REM sleep is important in memory

A

Depriving humans of REM sleep can impair their ability to learn tasks
Increased duration of REM sleep following intense learning

56
Q

What neurotransmitters do the brain stem modulatory neurons release during waking

A

NE and serotonin enhance the waking state

57
Q

How do the diffuse modulatory systems affect the thalamus

A

Control the rhythmic behaviour of the thalamus, which in turn controls many EEG rhythms of the cerebral cortex

58
Q

Why does sensory info to the cortex get blocked during deep sleep

A

Slow, sleep-related rhythms of the thalamus up to the cortex block the flow of sensory info

59
Q

How do the brain stem modulatory systems prevent movement during REM sleep

A

Descending branches of the diffuse modulatory systems inhibit motor neurons during dreaming

60
Q

What is the ascending reticular activating system

A

The region of the brainstem containing many sets of ascending modulatory systems- named by Moruzzi after brainstem lesion experiments

61
Q

What modualory system sets of neurons increase their firing anticipating awakening/during arousal

A

Locus coeruleus, raphe nuclei, basal forebrain and brainstem, midbrain, hypothalmus

62
Q

Modulatory systems-what does the locus coruleus release

A

NE

63
Q

Modulatory systems-what does the raphe nucleus release

A

Serotonin

64
Q

Modulatory systems-what does the basal forebrain and brain stem release

A

AChs

65
Q

Modulatory systems-what does the midbrain use as a neurotransmitter

A

Histamine

66
Q

Modulatory systems-what does the hypothalamus use as a transmitter

A

Hypocretin/orexin

67
Q

What do neurons of diffuse modulatory systems collectively synapse on

A

Directly synapse on the thalamus, cerebral cortex and many other regions

68
Q

What is the general effect of diffuse modulatory systems during arousal

A

Depolarisation of neurons, increasing neuronal excitability, suppressing rhythmic forms of firing

69
Q

What is hypocretin/orexin

A

A small peptide neurotrasmitter expressed mainly by neurons whose cell bodies are in the lateral hypothalamus

70
Q

What do the axons of hypocretin-secreting neurons project onto

A

Cells of the cholinergic, noradrenergic, serotonergic, dopaminergic and histaminergic modulatory systems

71
Q

Summarise the roles of hypocretin

A

Promotes wakefulness, inhibits REM sleep, facilitates neurons that enhance motor behaivour, regulates neuroendocrine systems

72
Q

What disorder often results from loss of hypocretin neurons

A

Narcolepsy

73
Q

What is narcolepsy

A

Excessive daytime sleepiness, cataplexy (sudden muscular paralysis while consciousness is maintainted ie REM sleep), sleep paralysis

74
Q

What happens to the firing rates of brain stem modulatory neurons when enter NREM sleep

A

General decrease in firing rate (NE, 5HT, ACh)

75
Q

What areas of the brain are more active durign REM sleep than waking

A

Extrastriate cortical areas, limbic system

76
Q

What neurotransmitter likely causes the thalamus and cortex to behave like they do in the waking state during REM sleep

A

ACh released by nuclei in the pons, increased at onset of REM sleep

77
Q

What is REM sleep behaviour disorder

A

Individuals act out their dreams due to disruption of the brain stem systems that usually mediate REM atonia

78
Q

What are some examples of sleep promoting factors

A

Adenosine, NO, interleukin 1, melatonin

79
Q

What suggests adenosine is a sleep promoting factor

A

Caffeine is an adenosine receptor antagonist
Administering adenosine increases sleep
Waking related changes in adenosine only occur in sleep-related regions

80
Q

What occurs to levels of NO and adenosine throughout the day

A

Levels progressively increase during waking periods and sleep deprivation, and gradually decrease during sleep

81
Q

How does adenosine exert its effects as a sleep promoting factor

A

Adenosine inhibits diffuse modulatory systems for ACh, NE and 5HT that promote wakefulness
May do so by disinhibiting the VLPO

82
Q

What is adenosine

A

Neuromodulator released by some neurons and glia, used to build DNA/RNA/ATP

83
Q

How does NO work as a sleep promoting factor

A

NO triggers adenosine release

84
Q

What suggests NO works as a sleep promoting factor (other than causing adenosine release)

A

Wake-promoting cholinergic neurons of the brain stem express particulalrly high levels of the enzyme for NO

85
Q

What cytokine has been suggested as a sleep promoting factor

A

Interleukin 1 synthesised by glia in the brain and macrophages- levels increase during waking, and peak before sleep onset, promoting NREM sleep even when not sick

86
Q

What is melatonin

A

A hormone secreted by the pineal body that is a derivative of the amino acid tryptophan

87
Q

Why is melatonin been called the ‘dracula of hormones’

A

Release is inhibited by light, released only when the envronment darkens (when we become sleepy in the evening), peaks in the early morning hours and falls to baseline when we awake

88
Q

What does melatonin do

A

Helps initiate and maintain sleep

89
Q

What are circadian rhythms

A

The daily cycles of daylight and darkness that result from the spin of the Earth

90
Q

What physiological and biochemical processes in the body rise and fall with daily rhythms

A

Body temp, blood flow, urine production, hormone levels, hair growth, metabolic rate

91
Q

What are zeitgebers

A

Environmental time cues that allow us to become entrained to day-night rhythms eg light/dark, temp

92
Q

Where i the SCN located

A

Consists of a tiny pair of neuron clusters in the hypothalamus, located either side of the midline bordering the third ventricle

93
Q

What tract provides RGC input

A

The retinohypothalamic tract

94
Q

Where does the SCN send output to

A

Primarily the hypothalamus, thalamus

95
Q

What is the neurotransmitter identity of SCN output neurons

A

GABA- presumably they inhibit the neurons they innervate

May rhythmically secrete neuromodulator vasopressin

96
Q

What is the 24 hour molecular cycle of the SCN based on

A

A negative feedback molecular cycle based on gene expression eg clock gebes

97
Q

What does CLOCK gene stand for

A

Circadian locomotor output cycles kaput

98
Q

Summarise how the negative feedback molecular cycle works in SCN

A

Genes are transcribed to produce mRNA and proteins
After a delay, proteins send feedback and interact with the transcription mechanism to decrease gene expression
Cycle lasts 24 hours

99
Q

How are cells in the body kept having a circadian rhythm?

A

Cells have their own circadian clock driven by the same gene transcriptino feedback loops driving the SCN clock, but these clocks are unde the control of the SCN

100
Q

What is the effect of the SCN influencing the ANS, body temp, hormones etc

A

Each of these processes regulates many of the body’s circadian clocks eg body temp effects the clocks of peripheral tissues

101
Q

How does the SCN control synthesis and secretion of melatonin

A

SCN projects to the pineal gland

102
Q

Which part of the brainstem promotes sleep

A

The ventrolateral preoptic nucleus VLPO

103
Q

How does the ventrolateral preoptic nucleus promote sleep

A

Sends GABAergic outputs to all major cell groups in the hypothalamus and brainstem involved in arousal, primarily active during sleep

104
Q

Where do orexin neurons have mutual projections with

A

VLPO neurons- orexin neurons reinforce the arousal system but don’t directly inhibit the VLPO

105
Q

Where does the VLPO receive inhibitory input from

A

Noraderaline and serotonin- the arousal systems it inhibits during sleep

106
Q

What is a flip-flop switch

A

A circuit with mutually inhibitory elements that sets up a self-reinforcing loop- activity in one side disinhibits itself by shutting down inhibition from the other side

107
Q

Why may sleep use a flip-flop circuit

A

Flip-flop circuits tend to avoid transitional states, as when one side begins to overcome the other the switch flips
Sleep-wake transitions ARE abrupt

108
Q

What is the result of one side of a flip-flop neural circuit being weakaned

A

Homeostatic forces cause the switch to ride closer to its transition point, meaning increased transitions between sleep/wake eg narcolepsy

109
Q

What is the result of adenosine reinfocing the arousal system via mutual VLPO projections

A

Stabilises the flip-flop switch

This may be why narcoleptic people, lacking orexin, have a destabilised flip-flop switch

110
Q

What is the DMH

A

The dorsomedial nucleus of the hypothalamus

111
Q

What dos the dorsomedial nucleus of the hypothalamus receive input from

A

SCN

112
Q

What output does the dorsomedial nucleus of the hypothalamus provide

A

One of the largest sources of output to the VLPO and orexin neurons, mainly GABAergic neurons

113
Q

What does the dorsomedial nucleus do

A

Integrates info from the SCN with feeding/temp etc, allowing circadian rhythms to be set at optimal phases for survival

114
Q

Does the dorsomedial nucleus promote or inhibit sleep

A

Promotes wakefulness by inhibiting sleep through GABAergic projections to the VLPO and orexin
Very active during wakefulness

115
Q

What genes are involved in the molecule cycle of gene expression underlying circadian rhythms

A

Circadian locomotor output cycles kaput (produces CLOCK), cryptochrome (produces CRY), period 1-3 (produces PER1-3), brain and muscle, ARNT-like (produces BMALI1)