Abstract
The original hypothesis that brain monoamine systems have a primary direct role in
depression has been through several modifications during the past 30 years. In order
to test this hypothesis and more fully characterize the role of serotonin and catecholamines
in the pathophysiology of depression and the mechanism of action of antidepressant
treatments, our research group has conducted a series of studies evaluating monoamine
depletion induced brief clinical relapse following different types of antidepressant
treatment of depressed patients. We have also studied the effects of monoamine depletion
(SD) on depressive symptoms in depressed and recovered patients off medication and
in healthy controls. Relapse to serotonin depletion or to catecholamine depletion
(CD) was found to be specific to the type of antidepressant treatment, i.e., patients
responding to selective serotonin reuptake inhibilitors relapsed more frequently following
SD than CD and patients responding to selective catecholamine reuptake inhibitors
relapsed more frequently following CD than SD. Neither CD or SD increased depressive
symptoms in clinically ill patients off treatment, or produced clinical depression
in normal controls. However, recovered patients with a prior history of depression
had a relapse with SD. Patients with obsessive compulsive disorder who improved on
SSRI treatment, did not have an increase in OCD symptoms but those with prior depressive
symptoms did have an increase in depressive symptoms with SD.
