Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts levodopa into dopamine. By blocking dopa decarboxylase, carbidopa increases the levels of levodopa that reach the brain, enhancing dopamine synthesis.

Another way drugs can impact neurotransmitter synthesis is by producing false transmitters. Methyldopa, for instance, is absorbed by adrenergic neurons and converted into α-methylnoradrenaline, a false transmitter. This compound displaces noradrenaline and alters receptor activation. It stimulates α₁ adrenoceptors less effectively but activates presynaptic α₂ receptors more efficiently, leading to an inhibitory feedback mechanism that reduces neurotransmitter production and release.

Certain neurotoxins, such as 6-hydroxydopamine and MPTP (1-methyl-4-phenyl-1,2,3,5-tetrahydropyridine), act as "Trojan horses" by being selectively taken up by neuronal junctions. Once inside, they transform reactive compounds that ultimately damage and destroy the nerve terminals—for example, 6-hydroxydopamine targets dopaminergic neurons, while MPTP affects dopaminergic and adrenergic neurons.

Additionally, a prodrug called droxidopa can cross the blood-brain barrier and is converted into noradrenaline by the enzyme dopa decarboxylase. This enhances sympathetic activity and can be used to treat conditions associated with low noradrenaline levels.

While drugs impacting neurotransmitter synthesis provide valuable insights into the modulation of adrenergic function, their clinical applications are often limited due to off-target effects and potential toxicity concerns.