ABSTRACT
The monoaminergic hypothesis of depression states that major depression could be related to a de˜- ciency of brain monoaminergic activity as depression responds to drugs that increase monoamine concentration in the synapses (Bunney and Davis 1965; Schildkraut 1965; Coppen 1967). Thus, treatment with monoamine reuptake inhibitors or monoamine oxidase (MAO) inhibitors induces clinical antidepressant activity, whereas treatment with the monoamine vesicular depletor reserpine produces a depressive syndrome.
