L5 Pharmacology of Sleep Flashcards

1
Q

What does ACh do in the ascending arousal system?

A

ACh from the LDT and PPT send signals to the thalamus to keep it active

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2
Q

Where are adenosine receptors in the brain?

A

They are located throughout the brain and block NT release (blockage of ACh = tiredness)

Many drugs interact with this process

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3
Q

What is the stimulant/sedation feedback loop?

A

Dependence on caffeine and nicotine in the morning to wake them up and have more throughout the day when the effects wear off
They then struggle to initiate/maintain sleep and rely on sedatives to help them get to sleep e.g. sleeping tablets and alcohol

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4
Q

What is the most widely used drug in the world?

A

Caffeine, and it comes in many forms
Coffee, chocolate, tea, fizzy drinks, energy drinks
Causes increased blood pressure, heart rate, increased anxiety via the ANS

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5
Q

How does caffeine work to promote wakefulness?

A

Caffeine’s molecular structure is very similar to adenosine so has the ability to bind to adenosine receptors as a competitive inhibitor
Adenosine is now no longer able to block cholinergic activity and therefore promotes wakefulness
If people rely on coffee in the long term, they may need to consume more to have the same benefits (tolerance)

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6
Q

What is caffeine’s affect on sleep?

A

It increases sleep onset latency, increases time spent in lighter stages of sleep, increases WASO, decreases in TST, decrease in sleep efficiency and an increase in day time dysfunction
Some studies show reduced REM sleep but it is dependent on duration and concentration of caffeine intake
Stimulating effects last for about 4 hours but stay in blood for longer as it metabolises slowly
People have different sensitivities due to metabolic rates

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7
Q

What happens with caffeine withdrawal?

A

Reduced sleep onset latency
Increased WASO
REM rebound
Increased TST - doesn’t necessarily mean good sleep quality

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8
Q

What mechanism does nicotine work through?

A

Addictive property of cigarettes
Nicotine also binds to nicotinic ACh receptors in the basal forebrain, activating them and producing excitation - increasing cholinergic activity and promoting wakefulness
Also releases dopamine activity as propagates to NAc, promoting wakefulness

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9
Q

What is nicotine’s effect on sleep?

A

Increased sleep onset latency, increased time spent in lighter stages of sleep, decreased SWS, decreased REM sleep, increased WASO, TST decreased

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10
Q

What happens with nicotine withdrawal?

A

Decreased sleep onset latency
Increased WASO
REM rebound
Increased TST

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11
Q

What did Colrain, Trindaer and Swan (2004) suggest about smoking cessation?

A

That cessation leads to SD, with sleepiness and dysphoria as side effects. This may result in smoking relapse to deal with these symptoms

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12
Q

How does alcohol work in the brain?

A

Potentially acts via increasing GABA activity and sedates the body
Other research predicts that it is involved with adenosine
Alcohol increases extracellular levels of adenosine, build up promotes sleepiness
Also alters synaptic functions of DA receptors in mesolimbic striatum causing increase in DA activity (Garcia & Salloum, 2015)

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13
Q

What happens in the night after alcohol consumption?

A

Individuals spend a lot of time in deep sleep in the early part of the night but this is just sedating yourself, it is not getting the natural biological sleep
Therefore all the benefits of SWS are not taking place
Alcohol metabolises quite quickly so wake up frequently during night, after sedative effects have worn off
Have a lot of REM sleep in second half
At low does alcohol reduces stage 3 NREM
Can worsen snoring and nightmare

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14
Q

What can be seen in alcohol withdrawal?

A

Increased sleep onset latency
Reduced SWS and increased REM rebound
Increased WASO
Reduced TST and efficiency (fragmented)

Lot of people go back to drinking so they actually sleep

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15
Q

How do we study cannabis’ effect on sleep?

A

Have to find people who are already actively using cannabis but these people often have additional addictive problems
Creates problems with quality of data
Also 60 different cannabinoids and a variety of ways to consume it - effects how it sits in your blood

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16
Q

What are the 2 most commonly explored compounds in cannabis?

A

Cannabidiol (CBD)
Tetrahydrocannabinol (THC)

Both act via CB1 receptors, linked to REM sleep

17
Q

How does CBD act on sleep?

A

Acts as an antagonist for CB1 receptors and blocks the GABA activity, leading to increased wakefulness

18
Q

How does THC act on sleep?

A

Acts as an agonist of CB1 receptors and therefore promotes sleepiness

This demonstrates why cannabis is so complex in sleep

19
Q

What does cannabis do in low doses?

A

Decreases sleep onset latency - acts as a sedative
Increases SWS
Decreases REM sleep
Increases TST

But still isn’t natural biological sleep

20
Q

What does cannabis do in high doses?

A

Increases sleep onset latency (stimulant)

Decreases SWS, REM sleep and TST

21
Q

What happens in cannabis withdrawal?

A
Seems to be really problematic
Increased sleep onset latency
Decreased SWS
Increased REM (strange dreams)
Decreased TST
Decreased sleep efficiency
22
Q

How do you restore healthy sleep patterns?

A

Can take months-years, if its even possible to do so due to the altered brain chemistry

23
Q

What are some treatments to reduce withdrawal effects?

A

Pharmacological therapy - but theres the potential for abuse
CBT
Mindfulness
Sleep Hygiene

24
Q

What is the quantification of sleep efficiency?

A

TST / time in bed x 100 (Garcia & Salloum, 2015)

25
Q

How does cocaine affect sleep?

A

Mainly through its effects on dopamine, leads to competitive inhibition of DAT in NAc and PFC - leading to increased DA in the cleft
Increased sleep onset latency
Decreased TST
Suppression of REM sleep