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The two most widely held biochemical models of depression-the catecholamine (CA) and indoleamine (lA) hypotheses-explain depression as a result of deficient transmission of the CA norepinephrine (NE) or the lA serotonin (5-hydroxytryptamine, 5-HT) respectively. Until recently, all drugs used to treat depression appeared to enhance neurotransmission in one or both of these systems, which was used to explain their antidepressant actions (Gelenberg and Klerman, 1978). In fact, it was this action of antidepressants that gave rise to the models of depression. Another way to increase brain levels of NE and 5-HT, and potentially to increase presynaptic activity, would be the systemic administration of the precursors of the neurotransmitters, an approach something like organic gardening in the brain. For this purpose, the 5-HT precursors tryptophan and 5-hydroxtryptophan (5-HTP), and the NE precursors tyrosine and dihydroxyphenylalanine (DOPA), have been administered to depressed patients. This paper reviews some of the theoretical background and clinical experience with the precursor strategy, focusing primarily on work with L-tyrosine. All four precursors a