Abstract
In a previous investigation we showed that large doses of DL-tryptophan (214 mg./kg. body weight) given to depressed patients receiving tranylcypromine (a monoamine oxidase inhibitor) potentiated the antidepressive effects of the drug (Coppen, Shaw and Farrell, 1963). This procedure increases the level of brain 5-hydroxytryptamine (5 HT) and tryptamine in the rat (Hess and Doepfner, 1961). Reserpine reduces the level of these amines in the brain, and it is known that patients being treated for hypertension with this drug often become depressed. Thus there is evidence that increasing certain brain amines may alleviate, and depleting brain amines may induce, a depressive illness. We therefore decided to study tryptophan metabolism in depressed patients. The pathways with which we were concerned are shown below.
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