Certain drugs inhibit the key enzymes involved in neurotransmitter synthesis. For instance, α-methyltyrosine blocks tyrosine hydroxylase, while carbidopa inhibits the dopa decarboxylase, essential for catecholamine synthesis. A few drugs, like methyldopa, are taken up by the adrenergic neurons and converted to α-methylnoradrenaline, a false transmitter. This α-methylnoradrenaline is stored in the synaptic vesicles instead of noradrenaline. Compared to noradrenaline, α-methylnoradrenaline has weaker effects on α1 -receptors but stronger effects on presynaptic α2-receptors. This triggers the inhibitory feedback mechanism, thus reducing neurotransmitter production and release. Neurotoxins, such as 6-hydroxydopamine and MPTP, undergo selective reuptake at neuronal junctions. They are converted into reactive, toxic compounds that can destroy nerve terminals. The prodrug droxidopa is converted by dopa decarboxylase to noradrenaline and potentiates sympathetic actions. Agents that interfere with noradrenergic synthesis have limited clinical scope due to their "off-target" effects and high toxicity.