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Welcome to 2 minute neuroscience, where I simplistically explain neuroscience topics
in 2 minutes or less.
In this installment I will discuss caffeine.
Caffeine is a stimulant drug and the most widely-consumed mind-altering substance in
the world.
It belongs to a class of compounds known as the methylxanthines, and is commonly found
in a number of natural sources including the seeds of coffee plants and the leaves of tea
plants.
Most of the effects of caffeine are thought to be traceable back to its action as an antagonist
at receptors for a neurotransmitter called adenosine.
This means that caffeine binds to adenosine receptors and blocks adenosine from binding
there and activating the receptor; thus, it reduces activity at the adenosine receptor.
Although there are 4 subtypes of the adenosine receptor, most of caffeine’s effects are
thought to be due to its antagonistic actions at the A1 and A2A subtypes.
Its ability to promote wakefulness may be especially due to actions at the a2a receptor
subtype.
How exactly the antagonism of the adenosine receptor translates into the effects of caffeine
is not completely clear.
Research suggests, however, that adenosine receptors are involved in promoting and regulating
sleep.
One way this is thought to occur is that adenosine activity can prompt the release of the neurotransmitter
GABA, which then inhibits neurons involved in arousal and wakefulness.
This promotes sleep, but when caffeine antagonizes adenosine receptors it opposes this action
and causes arousal.
Adenosine receptors are also thought to be involved in reducing the activity of a number
of neurotransmitters, including dopamine and norepinephrine, through methods ranging from
inhibiting neurotransmitter release to affecting neurotransmitter binding.
Thus, caffeine also blocks these effects, which may contribute to caffeine’s stimulating
and reinforcing actions.