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Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or
less.
In this installment I will discuss amphetamine.
Amphetamine is a stimulant drug used mainly in the treatment of ADHD.
Several popular drugs, like Adderall, primarily contain amphetamine.
Although we don’t have a full understanding of the effects of amphetamine on the brain,
there are some aspects of its pharmacology that are well established.
Amphetamine binds to the transporter proteins for monoamines like dopamine, norepinephrine,
and serotonin and then can be taken up into neurons via these transporter proteins.
Once inside the neuron, amphetamine disrupts the storage of monoamines in synaptic vesicles.
One way it does this is by inhibiting a protein called vesicular monoamine transporter
2, or VMAT2, whose normal role is to transport monoamines into vesicles.
Inhibition of VMAT2 leads to higher levels of these neurotransmitters in the neuron.
Through a mechanism or mechanisms that are still not fully understood, amphetamine is
then able to cause the monoamine transporter proteins to run in reverse, leading to the
increased release of monoamines---especially dopamine and norepinephrine---and increased
levels of these neurotransmitters in the synaptic cleft.
These elevated monoamine levels can have various effects on different parts of the central
nervous system.
Increased dopamine levels in the reward system, for example, may contribute to the reinforcing
effects of amphetamine use.
Although the primary action of amphetamine is to cause the increased release of monoamines,
there are various other mechanisms that may contribute to the effects of the drug.
For example, amphetamine also competes with monoamines for reuptake into the neuron, in
effect inhibiting reuptake.
And it may inhibit the activity of monoamine oxidase, an enzyme that metabolizes monoamines.
The effect of both of these actions is to additionally increase levels of monoamines
in the neuron and the synaptic cleft.