Neurobiology of sleep Flashcards

(52 cards)

1
Q

EEG records the difference in electrical conductivity between single neurons
T/F

A

False - signal from single neurons is too small to detect, so use a summation of several neurons in an area

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2
Q

________ neurons produce the strongest EEG signal because they are aligned and fire together

A

Pyramidal neurons

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3
Q

Before the invention of EEG, sleep was studied by_______

A

Observing behaviour

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4
Q

Bremer thought that sleep was caused by_______and found MISLEADING evidence for this__________

A

Sleep caused by a loss of consciousness;
cut top of mid brain - lost all sensory input, low EEG –> deep sleep state;
Cut top of spinal cord - kept some sensory input = conscious

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5
Q

Van economo (1930) found that the hypothalamus was a critical structure for sleep; person with insomnia is likely to have ________ whereas someone with day time sleepiness will likely have______

A

Insomnia - injury to the anterior hypothalamus

Sleepiness - injury to posterior hypothalamus

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6
Q

The hypothalamus is located in the________

A

midbrain

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7
Q

the thalamocortical loop involves ________ and moderates ________cycle

A
reticular formation (mid brain) + thalamus + cx 
sleep wake
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8
Q

Why are we less responsive during sleep compared to wake states?

A

Wake state has regular, rhythmic action –> more obvious when an external stimuli disrupts it. Whereas when it is in sleeping state, the rhythm is ALREADY disrupted = we are less likely to be conscious of another disruption

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9
Q

The ascending activation system consists of 2 networks__________

A

Cholinergic system + monoaminergic system

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10
Q

The cholinergic system regulates ____________

A

is responsible for the RHYTHMICITY, activation causes EEG DE-synchrony

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11
Q

The monoaminergic system is responsible for_________

A

Providing many inputs to the cortex to KEEP IT IN WAKE STATE

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12
Q

What are the 4 major monoaminergic inputs of the ascending activation system?

A

DA
5-HT
Histamines
Norepinepherine

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13
Q

In studies of arousal / cogmntive function the NT looked at MOST is;

a) DA
b) 5-HT
c) Norepinepherine
d) GABA

A

C - norepinepherine

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14
Q

NA is generated WHERE? and is released when encountering______

A

Locus coeruleus; when faced with stressor NA gets released = incr arousal

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15
Q

A lesion to the locus coeruleus will make Jimmy_________

A

Have INCR slow wave sleep + less aroused

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16
Q

Like NA, 5-HT is _________in wake state, _____ in NREM, and _______in REM

A

Wake - highly active
NREM - less
REM - off

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17
Q

5-HT are produced in _________

A

Raphe nuclei

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18
Q

SSRI’s affect sleep by_________

A

inhibiting reuptake of 5-HT –> INCR wakefulness + decease REM

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19
Q

Antihistamines affect sleeping cycle

T/F

A

FALSE - only affect sleep LATENCY, not sleep itself = affect waking cycle

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20
Q

Histamines are created WHERE?

A

tuberomammillary neurons

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21
Q

where is DA created?

A

Substantia nigra

Ventral tegmental area

22
Q

INCORRECT one is;

a) DA is concentrated in the substantia nigra
b) DA neurons don’t change firing rate across sleep/wake cycles
c) that DA increases when person stays awake for long periods
d) modafinil - drug acting on ]DA-ergic system improves cognitive function in sleep deprived clients

A

A - DA is widespread across the brain

23
Q

Lesion to the input areas for the thalamocortical loop will induce sleep T/F

A

FALSE - they are all important for wakefulness but are not CAUSALLY linked –> can induce sleepiness, but NOT sleep

24
Q

UNTRUE about orexin;

a) it is important for stabilisation of wakefulness
b) it is synthesised in the thalamus
c) destruction of orexin p/way causes devastating effects ion wakefulness
d) is important for metabolism / eating

A

B - is synthesised in the lateral HYPOTHALAMUS

25
What evidence d we have for role of orexin in wakefulness? metabolism?
Wakefulness - orexin / its receptors are DEFICIENT in those with narcolepsy metabolsim - those with narcolepsy eat LESS but have a greater BMI --> linked
26
Orexin is associated with _________ wakefulness behaviours
Reward system + food seeking
27
Lesion to the lateral hypothalamus induces sleep | T/F
False - orexin not CAUSALLY linked, will only make you SLEEPY
28
What is meant by an 'ascending neural system?
Info goes up into more complex areas of the brain to generate wakefulness
29
Why do we have SEVERAL wake systems instead of ONE universal one?
Bc being 'awake' is not in itself a function for survival, we need to seek reward, seek food, reproduce, etc., = separate systems for each goal
30
Cholinergic system involves LTD+PPT, these are both ______during wake/REM states and _______ during NREM
ACTIVE in wake/REM | Low in NREM
31
Blocking cholinergic neurons with drugs causes________
cholinergic neurons send signal for AROUSAL --> blocking with drugs = induce sleep
32
the *updated* version of the wake system's BACKBONE involves which NT's? Destcruction of these areas will be_________
GABA (inh-ory) glutamate (exc-ory) DA Destruction = INDUCE SLEEP
33
The wake system has 4 major systems;
a) cholinergic system b) monoaminergic system c) orexinergic system d) backbone
34
We have 3 major sleep centres_________
1) ventralateral preoptic area (VLPO) 2) median preoptic nucleus 3) parafacial zone
35
INCORRECT about VLPO is; a) it is the on/off switch for sleep b) it is located in the posterior hypothalamus c) Lesion to VLPO decrease in REM sleep d) has GABA + galanin projections that spread to all awake centres
B - it is located in the ANTERIOR hypothalamus. Is on during sleep --> if can't turn it on = insomnia.
36
There is no 'switch' for waking/sleeping state | T/F
FALSE - VLPO is sleep switch
37
The media preoptic nucleus is related to ________ stgae of the 2 process model and has highest activation in ___________
Homeostatic sleep load, regulates sleep. | Highest activation in evening --> when sleep load HIGH, falls during sleep when sleep debt is paid off
38
The parafacial zone works to inhibit_______ part of the wake system
the backbone
39
The wake maintenance zone occurs when_________
the sleep load is at its highest so the circadian system fights it by peaking at this time = high alertness between 6/9pm
40
Sleep regulation is governed by the actions of ___________
SCN - via indirect pathways (bc sends signals to sub par ventricular zone, DMH)
41
If the SCN receives inhibitory input, the outcome will be_____
Inducing sleep bc DMH sneds inh signal --> GABA --> switching on VLPO = sleep
42
If the SCN receives excitatory input, the outcome will be_____
DMH will send exc input to glutamate = orexinergic systems activate = WAKE state
43
Why do we look for objective markers of sleepiness?
safety i.e. driving, work safety
44
The two markers of heostatis sleep drive are_______
1) Adenosine levels in forebrain | 2) SWS
45
As the night progresses, we have ______SWS. The longer we are awake, the ______ we have SWS; therefore a nap will _______ the amount of SWS.
As the night progresses, we have LESS SWS. The longer we are awake, the MORE we have SWS; therefore a nap will DECREASE the amount of SWS.
46
What does the synaptic homeostasis suggest about learning
We learn new stuff every day = make new synaptic connections To incr efficiency, reduce space, SWS does SYNAPTIC DOWNSCALING to reduce number of connections = reducing intensity of connections may actually STRENGTHEN important signals by reducing NOISE
47
SWS occurs across all regions of the brain simultaneously T/F
FALSE - occurs in the areas used most that day, most SWS occurs in the PFC
48
Local sleep refers to____________
Sleep occurring in ONE area of the brain and not another. May occur both in waking and sleeping states
49
Sleep is a spatially and temporally uniform process | T/F
False
50
Adenosine is a biomarker of SWA, it ______ during wakefulness and _______ in sleep.
RISE in day, FALLS in sleep. | Builds up during the day in forebrain
51
Caffeine is an adonosine antagonist, this means_______
it takes up adenosine's receptors and blocks their effect --> keeps you ALERT
52
The Sleep promoting regions are________
VLPO, parafacial zone, Median preoptic area