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After reports in the late 1950s of a correlation between the effects of psychotropic drugs on mono-amine metabolism and on affective states, it became generally accepted that brain monoaminergic systems contributed to the pathophysiology of depression. After this, psychiatric researchers continued to pursue the neurochemical effects of antidepressants, hoping to gain novel insights into the biology of depression, what researchers themselves have referred to as the "pharmacological bridge." In this way, researchers repeatedly adapted their field's theoretical framework to fit conflicting evidence without challenging underlying and highly questionable assumptions concerning the specificity of psychotropic drug treatments. The result is a series of depression theories in which neuroplasticity theories are the most recent addition. The author uses Imre Lakatos's concept of "research program" to investigate this chronological sequence of theories. It is proposed that for over thirty years the pharmacological bridge provided direction to a psychiatric research program; more recently, however, the pharmacological bridge has come under siege as new laboratory technologies, such as neuroimaging, have increasingly replaced drugs as standard tools to investigate neuropathophysiology. Thus, this work illustrates how the epistemological and technological aspects of research intertwine in the history of psychiatry in general and the field of depression in particular.