1965

Schildkraut’s paper in Amer. J. Psychiat. formulates catecholamine hypothesis of depression (the amine theories): “The argument was that as reserpine was known to deplete catecholamines and as it was also known that reserpine could lead to depression and in some cases make people suicidal, there were strong suggestions that the depletion of catecholamines might be associated with the generation of depressive states. Because tricyclic antidepressants inhibited reuptake, it could be inferred that the effects of this would be to increase catecholamines in the synaptic cleft, thereby leading to a functional increase in the level of these neurotransmitters. Because the MAOIs also led to an increase in catecholamine levels, by blocking their metabolism, the inference was that both major groups of antidepressants led to increased amine levels. . . . this particular statement in 1965 came to dominate the field, set research agendas, and direct drug company efforts for the following two decades. It crystallized a split in psychiatry between biological and psychodynamic branches, each group having its own journals, its own meetings, and de facto very little to do with each other. Although the introduction of the drugs had thrown differences into relief, psychiatrists of all orientations could nevertheless use them. The catecholamine hypothesis, however, emphasized the advent of the psychiatric researcher who was conversant with the details of neurotransmitter metabolism, receptor binding, and endocrine changes – a researcher who spoke a different language from the analyst (Healy, 156- 157).