| History and evolution of the monoamine hypothesis of depression. | |
| | |
MedLine Citation:
|
PMID: 10775017 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
The symptoms of depression can be improved by agents that act by various mechanisms to increase synaptic concentrations of monoamines. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central noradrenergic and/or serotonergic systems and that targeting this neuronal lesion with an antidepressant would tend to restore normal function in depressed patients. The hypothesis has enjoyed considerable support, since it attempts to provide a pathophysiologic explanation of the actions of antidepressants. However, in its original form it is clearly inadequate, as it does not provide a complete explanation for the actions of antidepressants, and the pathophysiology of depression itself remains unknown. The hypothesis has evolved over the years to include, for example, adaptive changes in receptors to explain why there should be only a gradual clinical response to antidepressant treatment when the increase in availability of monoamines is rapid. Still, the monoamine hypothesis does not address key issues such as why antidepressants are also effective in other disorders such as panic disorder, obsessive-compulsive disorder, and bulimia, or why all drugs that enhance serotonergic or noradrenergic transmission are not necessarily effective in depression. Despite these limitations, however, it is clear that the development of the monoamine hypothesis has been of great importance in understanding depression and in the development of safe and effective pharmacologic agents for its treatment. |
| | |
Authors:
|
R M Hirschfeld |
Related Documents
:
|
12716247 - Lithium carbonate versus cognitive therapy as sequential combination treatment strategi... 18671467 - Desvenlafaxine succinate for the treatment of major depressive disorder. 10442787 - The place for the tricyclic antidepressants in the treatment of depression. 17254527 - Antidepressant use in ambulatory cancer patients. 326447 - The effects of prednisolone in leucocyte function in man. a double blind controlled study. 7841897 - An experimental evaluation of the effects of transcutaneous nerve stimulation (tns) and... |
Publication Detail:
|
Type: Historical Article; Journal Article; Review |
Journal Detail:
|
Title: The Journal of clinical psychiatry Volume: 61 Suppl 6 ISSN: 0160-6689 ISO Abbreviation: J Clin Psychiatry Publication Date: 2000 |
Date Detail:
|
Created Date: 2000-04-26 Completed Date: 2000-04-26 Revised Date: 2005-11-16 |
Medline Journal Info:
|
Nlm Unique ID: 7801243 Medline TA: J Clin Psychiatry Country: UNITED STATES |
Other Details:
|
Languages: eng Pagination: 4-6 Citation Subset: IM; Q |
Affiliation:
|
Department of Psychiatry and Behavioral Sciences, University of Texas Medical Branch, Galveston 77555-0188, USA. rohirsch@utmb.edu |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Adrenergic Uptake Inhibitors
/
history,
pharmacology,
therapeutic use Antidepressive Agents / history, therapeutic use Depressive Disorder / drug therapy*, physiopathology* Drug Industry History, 20th Century Humans Imipramine / history, pharmacology, therapeutic use Morpholines / history, pharmacology, therapeutic use Norepinephrine / antagonists & inhibitors, deficiency, physiology* Receptors, Biogenic Amine / antagonists & inhibitors, drug effects Serotonin / deficiency, physiology* |
| Chemical | |
Reg. No./Substance:
|
0/Adrenergic Uptake Inhibitors; 0/Antidepressive Agents; 0/Morpholines; 0/Receptors, Biogenic Amine; 50-49-7/Imipramine; 50-67-9/Serotonin; 51-41-2/Norepinephrine; 98769-81-4/reboxetine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Cardiac rotation and relaxation in patients with aortic valve stenosis.
Next Document: Depression: the case for a monoamine deficiency.