Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Depression: the case for a monoamine deficiency.

P L Delgado1

  • 1Department of Psychiatry, University of Arizona College of Medicine, Tucson 85724, USA. delgado@u.arizona.edu

The Journal of Clinical Psychiatry
|April 25, 2000
PubMed
Summary

The monoamine hypothesis of depression suggests neurotransmitter depletion, but evidence is lacking. Antidepressants require these systems, yet their deficiency

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Serotonin receptor, SERT mRNA and correlations with symptoms in males with alcohol dependence and suicide.

Acta psychiatrica Scandinavica·2011
Same author

Reboxetine: a review of efficacy and tolerability.

Drugs of today (Barcelona, Spain : 1998)·2003
Same author

Association between a serotonin transporter promoter region polymorphism and mood response during tryptophan depletion.

Molecular psychiatry·2002
Same author

Living with anxiety disorders: as good as it gets...?

Bulletin of the Menninger Clinic·2000
Same author

Tryptophan depletion and risk of depression relapse: a prospective study of tryptophan depletion as a potential predictor of depressive episodes.

Biological psychiatry·2000
Same author

Approaches to the enhancement of patient adherence to antidepressant medication treatment.

The Journal of clinical psychiatry·2000

Area of Science:

  • Neuroscience
  • Psychiatry
  • Pharmacology

Background:

  • The monoamine hypothesis of depression posits that reduced serotonin, norepinephrine, and dopamine levels cause depression.
  • Current antidepressants elevate these neurotransmitters, seemingly supporting the hypothesis.
  • However, direct evidence for primary monoamine system dysfunction in depression is scarce.

Purpose of the Study:

  • To investigate the role of monoamines in depression using a depletion paradigm.
  • To examine the necessity of intact monoamine systems for antidepressant efficacy.
  • To clarify the contribution of monoamine deficiency to the etiology of depression.

Main Methods:

  • Utilizing a monoamine depletion paradigm to experimentally manipulate neurotransmitter levels.
  • Observing the effects of depletion on depressive symptoms in patients and healthy volunteers.
  • Assessing the impact of depletion on antidepressant response.

Main Results:

  • Antidepressant response was transiently reversed by monoamine depletion, dependent on the drug class.
  • Monoamine depletion did not worsen symptoms in unmedicated depressed patients.
  • Depression was not induced in healthy volunteers by monoamine depletion.

Conclusions:

  • Antidepressant medications require functional monoamine systems for therapeutic effects.
  • The precise role of monoamine deficiency in the pathophysiology of depression remains debated.
  • Further research is needed to fully understand the complex etiology of depression.

Related Experiment Videos