This is applicable with amphetamine (Vyvanse too) methamphetamine but also fluorinated ones or even MDMA, MDA and benzofurans (but in this case I'm going to talk about amphetamine specially):

Amphetamine is a small molecule but despite being so small it exerts the release of almost all of the neurotransmitters known in your body, the phenethylamine structure slightly changed with a methyl proup allows it to pass the blood brain barrier due to its lypophilicity and the it enters inside the presynaptic button thru monoamine transporters like DAT, NET or SERT but without being oxidized by the MAO enzyme, that is the case that happens with phenethylamine (also DMT but we're talking about amps)

When it enters the presynaptic neuron it basically starts to change the natural physiological mechanism to the point of making the presynaptic button to work in a completely different way that will produce the highest amounts of neurotransmitters to be released into the synaptic cleft.

So after entering it does a few things that will completely alter the presynaptic button mechanism of neurotransmission:

1.VMAT1 and VMAT2 agonism: Activation of the vesicular monoamine transporter means that amines, (specially dopamine and norepinephrine but also norepinephrineand histamine) will pass from being dissolved in the cytosol of the presynaptic button to start forming vesicules. In the case of dopamine as a example, it will start to concentrate in this vesicules and will be released via exocytosis to the synaptic cleft, this process happens naturally too but with amphetamine it happens much faster, increasing dopamine concentration in the synaptic cleft

2.TAAR1: When amphetamine binds to this receptor it lnduces a chain of reactions that will phosphorylate dopamine, norepinephrine and serotonin transporters making them act in a completely different way. When phosphorylation happens transporters stop working so there is an inhibition in the reuptake of monoamines but some of this transporters like DAT reverses the mechanism of action instead of internalizing when they phosphorylate, meaning that instead there is an efflux of dopamine increasing dopamine concentration in the synaptic cleft

3.MAO inhibition: In high doses amphetamine inhibits the enzyme that oxidizes the excess of dopamine, norepinephrine and serotonin so they will start to accumulate even more because most of this enzymes are inhibited therefore not cleaning the excess of neurotransmitters

With this mechanisms of action amphetamine bassically end up increasing concentrations of dopamine, norepinephrine, serotonin and histamine but it's also known that amphetamine increases to a lesser extent adrenaline CART-peptides, endogenous opioids, corticosteroids, adrenocorticotropic hormone and glutamate