Abstract

Some patients develop depressive symptoms when treated with reserpine^{1 2} or tetrabenazine,³ which deplete the brain of the three monoamines, dopamine, noradrenaline and 5-hydroxytryptamine (serotonin). Thus, defective transmission in some central noradrenergic or serotonergic pathways has been invoked as the possible physiological change underlying depressive symptoms. In line with this hypothesis, most effective anti-depressive drugs (e. g. amitriptyline and imipramine) block the re-uptake of one or more monoamines (including dopamine to some extent) and may thus potentiate transmission in these pathways. Most attention has focused on noradrenaline and serotonin. Studies of dopamine, however,⁴ indicate that its turnover may be reduced, particularly in depressed patients with marked psychomotor retardation. Since ascending dopaminergic pathways may function as components of the central mechanisms of reward⁵ and depressed patients gain little satisfaction from life, it is plausible that a lack of dopamine at the postsynaptic site may be associated with some depressions, or some particular features of depression.