Sleep - pharmacology of sleep

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We have an intricate network of neurotransmitters involved in regulating sleep-wake cycle. These are absolutely fundamental to regulating our sleep-wake behaviour. so...
Any changes or alterations to levels of these neurotransmitter can have a significant impact on the sleep-wake cycle.
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When you’re wide awake the activity in your brain should look something like this:
Coordinated activity of interconnected ascending arousal system.Excitatory(wake-promoting)neurotransmitters:Acetylcholine.Dopamine.Histamine.Noradrenaline.Serotonin.These are the transmitters which keep us awake (Schwartz & Roth, 2008)
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Wake promoting neuromodulator
-Hypocretin (also known as orexin) Synthesised in a small group of cells in the lateral and posterior hypothalamus (Schwartz & Roth, 2008)
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Noradrenaline Serotonin Histamine Acetylcholine Dopamine Orexin (hypocretin)...
Innervate the cortical regions
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Acetylcholine From LDT and PPT...
Send signals to the thalamus
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Adenosine -->
Adenosine receptors located throughout the brain --> Block neurotransmitter release (Schwartz & Roth, 2008)
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ATP
ATP is the brains metabolic currency. Throughout the day ATP is metabolised and broken down into adenosine.
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Adenosine
Adenosine builds up throughout the day (sleep pressure). It acts via Adenosine receptors. Upon activation these receptors block neurotransmitter release in particular cholinergic neurons in the basal forebrain.
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Primary inhibitory (sleep-promoting) system
Located in the ventrolateral preoptic area of the hypothalamus (VLPO) Inhibits arousal system (Schwartz & Roth, 2008)
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VLPO
VLPO is the sleep promoting area, but very importantly is it inhibits the neurotransmitters involved in arousal. (Schwartz & Roth, 2008)
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The inhibitory neurotransmitters include:
-GABA -Galanin (Schwartz & Roth, 2008)
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Stimulant/sedation feedback loop
Waking day for many is fuelled by caffeine/nicotine.But they can last in the body for some time.So when time to go to sleep-feel alert.So may resort to alcohol/sleeping tablets.But,this way some benefits of sleep impaired.So,next day need stimulants
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***Ogeil & Phillips, 2015***
Being dependent on caffeine has been found to cause poor sleep quality, day‐time dysfunction, and increased sleep disturbances
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***Mechanisms of action with caffeine - adenosine***
Adenosine act via adenosine receptors and it makes us feel sleepy. Activation of adenosine receptors leads to blocking excitatory neurotransmitter activity (Boutrel & Koob, 2004)
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***Mechanisms of action with caffeine - caffeine***
Caffeine has a similar structure to adenosine. It binds to adenosine receptors resulting in inhibition. Adenosine can no longer act via its receptor and block neurotransmitter release. Therefore we stay awake (Boutrel & Koob, 2004)
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***Caffeine - sleep onset latency***
Increased (Teofilo, 2008b). Caffeine increases arousal therefore in take longer to fall asleep.
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Caffeine - time spent in lighter stages of sleep
Increased time spent in lighter stages of sleep
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Caffeine - SWS
reduced time in SWS.However,some studies have shown an increase in SWS&this is likely to do with disrupted sleep as a result of caffeine consumption,which means individuals feel more tired the next day,this can often lead to more time spent in SWS
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Caffeine - REM sleep
Some studies have shown a decrease in REM sleep due to increased arousal and sleep fragmentation. However, others have shown no change in REM.
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Caffeine - wake after sleep onset
Increased
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***Caffeine - total sleep time***
Decreased (Teofilo, 2008b)
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Caffeine - sleep efficiency
Decreased.
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***Haskell et al., 2005***
Caffeine has been shown to improve attention, reaction time, working memory and mood
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***Haskell et al., 2005 - background***
If you have been sleep deprived caffeine can reverse the effects of sleep deprivation. It’s important to appreciate that caffeine is restoring performance degraded by sleepiness not producing superior performance.
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***Caffeine withdrawal - sleep onset latency***
Decreased (Jaehne et al., 2009)
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***Caffeine withdrawal - wake after sleep onset***
Increased (Teofilo, 2008b)
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***Caffeine withdrawal - REM (rebound)***
Increased (Liu et al., 2013). Whilst consuming caffeine REM can be reduced, therefore during withdrawal individuals often spend more time in REM- this is called REM rebound.
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***Caffeine withdrawal - total sleep time***
Increased (Teofilo, 2008b)
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***Stolerman & Jarvis, 1995***
Over 4000 chemicals in cigarette smoke. It’s well known that nicotine is a major in tobacco smoke which is responsible for addition
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Caffeine is a ...
stimulant
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Nicotine is a...
Stimulant
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***Nicotine - mechanisms of action - cholinergic activity***
In the basal forebrain we get cholinergic activity- acetylcholine acts via its own receptors and upon binding it open the pore enabling the influx of ions causing depolarization and excitation- keeping you awake (Boutrel & Koob, 2004)
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***Nicotine - mechanisms of action - nicotine***
Nicotine promotes wakefulness by stimulating cholinergic neurotransmission in the basal forebrain. Nicotine activates acetylcholine receptors which also bind with nicotine (nAchR) (Boutrel & Koob, 2004)
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***Nicotine - mechanisms of action - dopamine - (Boutrel & Koob, 2004)***
Once these receptors are activated they enable ions to pass through which initiates an action potential,this action potential propagates&travels to nucleus accumbens,activating the reward circuits in the brain which results in the release of dopamine
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***Nicotine - mechanisms of action - This cholinergic and dopaminergic activity leads to...***
Increased arousal (Boutrel & Koob, 2004)
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***Nicotine - sleep onset latency***
Increased (Teofilo, 2008b)
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Nicotine - time spent in lighter stages of sleep
Increased. Spending more time in lighter stages of sleep means you getting less time in deep sleep
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***Nicotine - SWS***
Decreased (Teofilo, 2008b)
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Nicotine - REM sleep
Some studies have found a decrease in REM sleep, others have found no change.
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Nicotine - wake after sleep onset
Increased
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***Nicotine - total sleep time***
Decreased (Teofilo, 2008b). Overall sleep efficiency is reduced.
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***Nicotine withdrawal - sleep onset latency***
Decreased (Jaehne et al., 2009)
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***Nicotine withdrawal - wake after sleep onset***
Increased (Teofilo, 2008b). Withdrawal effects lead to increased WASO.
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***Nicotine withdrawal - REM (rebound)***
Increased (Liu et al., 2013)
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***Nicotine withdrawal - total sleep time***
Increased (Teofilo, 2008b)
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Colrain, Trindaer & Swan (2004)
Model-shows smoking cessation leads to sleep disruption,which can contribute to sleepiness&dysphoria.Acknowledges the possibility of smoking cessation leading directly to sleepiness&dysphoria too.Sleepiness &dysphoria can then lead to smoking relapse
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Alcohol has both...
stimulating and sedative effect
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Alcohol
The literature in this field is complex- underlying mechanisms are not completely understood.
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***Alcohol and GABA***
Studies have proposed that GABA&alcohol may act via GABAA receptors, similar to benzodiazepines, which are hypnotics that induce sleep [reviewed in Wallner et al., 2006]. Thus, activation of GABAA receptors by alcohol may lead to sleep promotion.
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***Alcohol and GABA - however...***
However, the effects of alcohol on GABAA receptors are complex and not completely understood [reviewed in Aguayo, Peoples, Yeh, & Yevenes, 2002;
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Alcohol - mechanisms of action - adenosine
Adenosine binds to adenosine receptors, decreasing release of neurotransmitters involved in promoting wakefulness. As a result you feel tired
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***Alcohol - mechanisms of action - alcohol***
Alcohol increases extracellular levels of adenosine. More adenosine means increase adenosine receptor activity and feeling more sleepy (Boutrel & Koob, 2004)
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Stradling (1993)
Alcohol - effects on sleep- First half of night - more SWS sleep. 2nd half of night - more wakefulness and more REM
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***Alcohol - first half of night - sleep onset latency***
Decreased (Ebrahim et al., 2013)
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***Alcohol - first half of night - SWS***
Increased (Brower, 2001)
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***Alcohol - first half of night - REM sleep***
Decreased (Ebrahim et al., 2013)
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Alcohol - second half of the night - REM (rebound) sleep
Increased
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Alcohol - second half of the night - wake after sleep onset
Increased
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***Alcohol - first and second halves of the night***
Because alcohol is metabolised quickly, its effects on the second half of sleep differ, with an increase in arousal and sleep fragmentation. It’s sedative effects wear off in the second half of the night resulting in arousal (Stradling, 1993)
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***Alcohol - withdrawal - sleep onset latency***
Increased (Gann et al., 2004)
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***Alcohol - withdrawal - SWS***
Decreased (Teofilo, 2008b)
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***Alcohol - withdrawal - REM (rebound) sleep***
Increased (Gann et al., 2004)
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***Alcohol - withdrawal - wake after sleep onset***
Increased (Teofilo, 2008b)
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***Alcohol - withdrawal - total sleep time***
Decreased (Gann et al., 2004)
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***Alcohol - withdrawal - sleep efficiency***
Decreased (Gann et al., 2004)
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Alcohol withdrawal
These problems with sleep usually lead individuals to relapse.
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***Throughout the day ATP is ...***
metabolised and broken down into adenosine (Fredholm et al., 1999)
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***Adenosine acts via...***
adenosine receptors (Boutrel & Koob, 2004)
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Adenosine acts via adenosine receptors. Upon activation these receptors...
block neurotransmitter release in particular cholinergic neurons in the basal forebrain (Boutrel & Koob, 2004)
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***Alcohol increases ...***
extracellular adenosine levels- increasing adenosine receptor activity which leads to increased sleepiness (Thakkar et al., 2015)
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***Caffeine blocks...***
adenosine receptor activity reducing sleepiness (Boutrel & Koob, 2004)
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***Nicotine increases ...***
cholinergic neurotransmission which has a stimulating effect (Boutrel & Koob, 2004)
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***The cannabis plant contains over ...***
60 cannabinoids (Garcia & Solloum, 2015)
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Cannabis - mechanisms of action - two compounds that looking at
Cannabidiol (CBD) and Tetrahydrocannabinol (THC)
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***Cannabis - mechanisms of action - Is Cannabidiol (CBD) antagonist or agonist at CB1 receptors?***
Antagonist (Pertwee, 2008)
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***Cannabis - mechanisms of action - Is Tetrahydrocannabinol (THC) antagonist or agonist at CB1 receptors?***
Agonist (Pertwee, 2008)
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***Cannabis - mechanisms of action - CBD and THC both act via...***
cannabinoid receptors in the brain- CB1 receptors (Pertwee, 2008)
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***Cannabis - mechanisms of action - CB1-receptors are linked to ...***
REM sleep and are found in high concentrations in the frontal cortex, the cerebellum and the basal ganglia (Schierenbeck et al., 2008)
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***Cannabis - mechanisms of action - The CB-1 receptors activate ...***
a variety of signal transduction pathways and interact with numerous neurotransmitters and neuromodulators (Schierenbeck et al., 2008)
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***CBD:***
blocks CB1 receptor activity, leads to increase wakefulness/alertness (Nicholson et al., 2004)
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***THC:***
activates CB1, leads to increase in sleepiness (Murillo-Rodríguez, 2008)
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***Nicholson et al., 2004***
The combination of THC with cannabidiol results in an increase in wakefulness compared to THC alone
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***Conroy & Arnedt, 2014***
research in cannabis has been limited by methodological factors such as tmarijuana dose, dosage timing, preparations of marijuana (e.g., THC vs. marijuana extract), and amount of participants' prior drug experience.
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***When Cannabis is in a low dose it is a...***
Sedative (Garcia & Salloum, 2015)
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When Cannabis is in a high dose it is a...
Stimulant
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**Cannabis - low dose - sleep onset latency***
Decreased (Teofilo, 2008b) People might smoke cannabis to relax, wind down and to get to sleep.
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***Cannabis - low dose - SWS***
Increased (Teofilo, 2008b)
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***Cannabis - low dose - REM sleep***
Decreased (Teofilo, 2008b)
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***Cannabis - low dose - total sleep time***
Increased (Teofilo, 2008b)
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***Cannabis - high doses - sleep onset latency***
Increased (Teofilo, 2008b)
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***Cannabis - high doses - SWS***
Decreased (Teofilo, 2008b)
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***Cannabis - high doses - REM sleep***
Decreased (Teofilo, 2008b)
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Cannabis - high doses - total sleep time
decreased
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***Cannabis - withdrawal - sleep onset latency***
Increased (Teofilo, 2008b)
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Cannabis - withdrawal - SWS
Decreased (Schierenbeck et al., 2008)
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***Cannabis - withdrawal - REM sleep (strange dreams)***
Increased (Moussas et al., 2009). Strange dreams generally occur with discontinuation of cannabis use (Schierenbeck et al., 2007)
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***Cannabis - withdrawal - total sleep time***
Decreased (Teofilo, 2008b)
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***Cannabis - withdrawal - sleep efficiency***
Decreased (Bolla et al., 2008)
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Sleep problems may lead to...
Cannabis relapse
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Sleep problems may lead to...
Cannabis relapse
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Treatments to reduce withdrawal effects
Pharmacological therapy, cognitive behavioural therapy, mindfulness and sleep hygiene
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***Conroy & Arnedt, 2014***
Physicians may be hesitant to pre-scribe pharmacotherapy because of their abuse potential, withdrawal effects, and potential for overdose if mixed with alcohol.
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***Howland, 2014***
Pharmacological treatment - Gabapentin has been found to be useful in treating insomnia in abstinent alcohol- dependent outpatients and appears to be safe
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***Brower et al., 2011***
A study found giving the melatonin receptor agonist ramelteon nightly to recovering alcoholic patients lead to a reduction of scores on an insomnia questionnaire,reduction in latency to sleep, and 1 additional hour of total sleep time
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***Treatments to reduce withdrawal effects - cognitive behavioural therapy***
includes developing behavioural and cognitive strategies to consolidate night time sleep (Conroy & Arnedt, 2014)
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Treatments to reduce withdrawal effects - mindfulness
Research is in it's early days but positive effects of mindfulness on sleep have been found in the literature (e.g. Howell et al., 2008)
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Ong et al., 2008 - found
Study that looked at mindfulness with cognitive-behavior therapy for insomnia.Found significant improvements in several symptoms of insomnia&decreases in pre-sleep arousal,sleep effort&dysfunctional sleep-related cognitions
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Ong et al., 2008 - Also,a significant correlation was found...
between the number of mindfulness sessions&changes on a trait measure of arousal.
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Summary - The neural basis of sleep is affected by the use of
stimulants/sedatives.
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Summary - The neural basis of sleep is effected by the use of stimulants/sedatives. Consequently these has an impact on:
Sleep onset SWS REM sleep. Total sleep time
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Summary - There is a differential effect on sleep during periods of:
Intoxication. Withdrawal
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***Wetter et al., 1995 - background***
Investigated the impact of tobacco withdrawal on sleep parameters.
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***Wetter et al., 1995 - participants***
Pp's who were cigarette smokers&were motivated to quit were given either nicotine patches or placebo patches while quitting
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***Wetter et al., 1995 - method***
Polysomnographic data was recorded for 2 precessation nights&3 postcessation nights.
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***Wetter et al., 1995 - results***
It was found that for dependent smokers, tobacco withdrawal increases sleep disturbance & nicotine replacement leads to postcessation improvements in polysomnographic measures of sleep quality (sleep fragmentation, Stage 3 and Stage 4 sleep).
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***Cottler et al., 1993)
When people are withdrawing from cocaine they also experience unpleasant dreams
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Card 2

Front

When you’re wide awake the activity in your brain should look something like this:

Back

Coordinated activity of interconnected ascending arousal system.Excitatory(wake-promoting)neurotransmitters:Acetylcholine.Dopamine.Histamine.Noradrenaline.Serotonin.These are the transmitters which keep us awake (Schwartz & Roth, 2008)

Card 3

Front

Wake promoting neuromodulator

Back

Preview of the front of card 3

Card 4

Front

Noradrenaline Serotonin Histamine Acetylcholine Dopamine Orexin (hypocretin)...

Back

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Card 5

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Acetylcholine From LDT and PPT...

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