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The revised monoamine theory of depression: a
modulatory role for monoamines, based on new findings from monoamine
depletion experiments in humans.
Heninger
GR, Delgado
PL, Charney
DS.
Department of Psychiatry, Yale University, New Haven,
CT, USA.
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.
The findings that relapse during treatment is specific to the type of
treatment and type of depletion, that neither SD or CD produced an
increase in clinical depression in healthy controls or depressed
patients off medication, and that recovered patients off medication have
a return of symptoms following SD, forces a major revision of the
current monoamine theories of depression. The new hypothesis most
consistent with this new data is that the monoamine systems are only
modulating "other" brain neurobiologic systems which have a more primary
role in depression. The modulatory or "antidepressant" function of the
monoamine systems appears to be only necessary during drug induced
recovery and the maintenance of recovery after a prior episode. These
clinical studies point to the need for more fundamental research on the
interaction of monoamine systems with other brain neurobiologic
mechanisms relevant to depression.
Publication Types:
PMID:
8852528 [PubMed - indexed for MEDLINE]
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