5. Pharmacology of Sleep Flashcards
sleep wake regulation
- ATP = brains metabolic currency
- ATP is metabolised throughout the day creating a build up of adenosine in the basal forebrain
- adenosine receptors are activated blocking excitatory neurotransmitters (in particular cholinergic neurons)
- leaves us feeling sleepy
ventrolateral preoptic nucleus (VLPO)
- sleep promoting area, inhibiting neurotransmitters involved with arousal
- inhibitory neurotransmitters = GABA and galamin
- when activated, they block excitatory neurotransmitters = sleep
stimulation-sedation feedback loop
- wake up and use stimulants (e.g. caffeine)
- too alert to sleep so use alcohol or sleeping tablets but that leads to a poorer nights sleep
caffeine use
- most widely used drug worldwide
- caffeinism has other effects such as increased HR, mood changes, anxiety
- similar molecular structure to adenosine so it binds and competes for the same receptors
- antagonistic nature makes you feel more alert
- adenosine is an agonist, caffeine stops the build up of adenosine and increases your alertness
- people metabolise it at different rates (can stay in your blood > 4h)
- can be used as a tool to combat sleep deprivation (ST) by increasing RT, alertness, WM mood – moderation can be good but not to depend on it
what is affected in the sleep cycle when having caffeine
INCREASE
- sleep onset latency
- time in light stages (less SWS) - some have shown to have more SWS due to a disrupted sleeping pattern the night previous
- wake after sleep onset (anxiety, HR)
DECREASED
- total sleep time
- REM
- sleep efficiency
SWS and REM = LT effects?
caffeine withdrawal
REDUCED
- sleep onset latency
INCREASED
- wake after sleep onset (due to physiological response)
- REM rebound
- overall sleep time increased but this may not be good quality sleep
nicotine use
- 4000 chemicals in cigs but nicotine is the addictive substance people must maintain
- stimulant similar to caffeine but acts differently targeting cholinergic activity in basal forebrain
- Ach acts via its own receptors and upon binding it opens the pore enabling an influx of ions causing depolarisation of cell with excitatory effects
- nicotine increases arousal by stimulating cholinergic activity
- can have direct effects or indirect effects
direct affects of nicotine
nicotine activates acetylcholine receptors which also bind with nicotine (nAchR) = depolarisation = more excitation
indirect affects of nicotine
once receptors are activated they enable ions to pass through which initiates an AP
- this then travels to the nucleus accumbens activating reward circuits in the brain (DA)
what is affected in the sleep cycle when having nicotine
INCREASE
- sleep onset latency
- more time in light stages
- more wakes after sleep onset
DECREASE
- less SWS
- less REM (not solid finding)
- total sleep time
nicotine withdrawal
INCREASE
- wake after onset increased
- REM rebound
- total sleep time increased (but might not be good quality - fragmented
DECREASE
- sleep onset latency
- affects day to day life like mood
nicotine cessation (end)
Colrain, Trindaer and Swan (2004)
- stopping smoking possibly you feel more sleepy and can also lead to dysphoria (restlessness, irritability)
- it also has direct impacts on sleep, poor sleep also increases sleepiness and dysphoria which could all lead to a relapse
alcohol use
- both stimulating and sedative effects
- stimulating effects are through excitatory transmission but general effects are sedative
- research here is complicated because the underlying mechanisms are not fully understood
- it is thought that the sedative effects come from GABA activity but this may not be the primary method of action
- adenosine is thought to increase extracellularly, building up and binding to receptors, decreasing the release of excitatory neurotransmitters related to maintaining wakefulness
what is affected in the sleep cycle when having alcohol
INCREASE
- time in SWS during first half of night (sedation not sleep)
- wake after onset increases during second half of night as the alcohol is metabolised relieving sedative effects
- more time in REM
DECREASE
- don’t feel rested next day = hangover
First half of night = SOL decreased, REM decreased and SWS increased
second half of night = REM rebound (more) and WASO increased
alcohol withdrawal
INCREASED
- sleep onset latency (changed physiology due to addiction)
- REM increased
DECREASE
- SWS due to REM rebound
- quality of sleep is fragmented (related to anxiety and other withdrawal symptoms)
- total sleep time and efficiency
- depends on how much and how long you were addicted for
