Role of serotonin in the pathophysiology of depression: focus on the serotonin transporter.

Role of serotonin in the pathophysiology of depression: focus on the serotonin transporter. Abstract Considerable evidence has accrued in the last two decades to support the hypothesis that alterations in serotonergic neuronal function in the central nervous system occur in patients with major depression. These findings include the following: (a) reduced cerebrospinal fluid (CSF) concentrations of 5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of serotonin (5-HT) in drug-free depressed patients; (b) reduced concentrations of 5-HT and 5-HIAA in postmortem brain tissue of depressed and (or) suicidal patients; (c) decreased plasma tryptophan concentrations in depressed patients and a profound relapse in remitted depressed patients who have responded to a serotonergic antidepressant when brain tryptophan availability is reduced; (d) in general, all clinically efficacious antidepressants augment 5-HT neurotransmission following chronic treatment; (e) clinically efficacious antidepressant action by all inhibitors of 5-HT uptake; (f) increases in the density of 5-HT2 binding sites in postmortem brain tissue of depressed patients and suicide victims, as well as in platelets of drug-free depressed patients; (g) decreased number of 5-HT transporter (determined with (3H)imipramine or (3H)paroxetine) binding sites in postmortem brain tissue of suicide victims and depressed patients and in platelets of drug-free depressed patients. In our studies, this reduction in platelet 5-HT transporter binding is not due to prior antidepressant treatment of hypercortisolemia and is not observed in mania, Alzheimer disease, schizophrenia, panic disorder, fibromyalgia, or atypical depression. In a pilot study, this deficit predicted treatment response to an experimental antidepressant. These findings support the hypothesis that alterations in 5-HT neurons play a role in the pathophysiology of depression. © 1994 The American Association for Clinical Chemistry « Previous | Next Article » Table of Contents This Article Clinical Chemistry February 1994 vol. 40 no. 2 288-295 » Abstract PDF Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Download to citation manager Responses No responses published Citing Articles Load citing article information Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Owens, M. J. Articles by Nemeroff, C. B. Search for related content PubMed PubMed citation Articles by Owens, M. J. Articles by Nemeroff, C. B. Related Content Load related web page information Follow Us Clinical Chemistry Trainee Council Register Today! www.traineecouncil.org Information for Authors Submit a Manuscript Editorial Board Clinical Case Studies Clinical Chemistry Guide to Scientific Writing Journal Club Podcasts Translated Content Annual Meeting Abstracts Permissions and Reprints Advertising Copyright © 2012 by the American Association for Clinical Chemistry http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Chemistry American Association for Clinical Chemistry

Role of serotonin in the pathophysiology of depression: focus on the serotonin transporter.

Clinical Chemistry, Volume 40 (2): 288 – Feb 1, 1994

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Publisher
American Association for Clinical Chemistry
Copyright
Copyright © 1994 by the American Association for Clinical Chemistry.
ISSN
0009-9147
eISSN
1530-8561
Publisher site
See Article on Publisher Site

Abstract

Abstract Considerable evidence has accrued in the last two decades to support the hypothesis that alterations in serotonergic neuronal function in the central nervous system occur in patients with major depression. These findings include the following: (a) reduced cerebrospinal fluid (CSF) concentrations of 5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of serotonin (5-HT) in drug-free depressed patients; (b) reduced concentrations of 5-HT and 5-HIAA in postmortem brain tissue of depressed and (or) suicidal patients; (c) decreased plasma tryptophan concentrations in depressed patients and a profound relapse in remitted depressed patients who have responded to a serotonergic antidepressant when brain tryptophan availability is reduced; (d) in general, all clinically efficacious antidepressants augment 5-HT neurotransmission following chronic treatment; (e) clinically efficacious antidepressant action by all inhibitors of 5-HT uptake; (f) increases in the density of 5-HT2 binding sites in postmortem brain tissue of depressed patients and suicide victims, as well as in platelets of drug-free depressed patients; (g) decreased number of 5-HT transporter (determined with (3H)imipramine or (3H)paroxetine) binding sites in postmortem brain tissue of suicide victims and depressed patients and in platelets of drug-free depressed patients. In our studies, this reduction in platelet 5-HT transporter binding is not due to prior antidepressant treatment of hypercortisolemia and is not observed in mania, Alzheimer disease, schizophrenia, panic disorder, fibromyalgia, or atypical depression. In a pilot study, this deficit predicted treatment response to an experimental antidepressant. These findings support the hypothesis that alterations in 5-HT neurons play a role in the pathophysiology of depression. © 1994 The American Association for Clinical Chemistry « Previous | Next Article » Table of Contents This Article Clinical Chemistry February 1994 vol. 40 no. 2 288-295 » Abstract PDF Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Download to citation manager Responses No responses published Citing Articles Load citing article information Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Owens, M. J. Articles by Nemeroff, C. B. Search for related content PubMed PubMed citation Articles by Owens, M. J. Articles by Nemeroff, C. B. Related Content Load related web page information Follow Us Clinical Chemistry Trainee Council Register Today! www.traineecouncil.org Information for Authors Submit a Manuscript Editorial Board Clinical Case Studies Clinical Chemistry Guide to Scientific Writing Journal Club Podcasts Translated Content Annual Meeting Abstracts Permissions and Reprints Advertising Copyright © 2012 by the American Association for Clinical Chemistry

Journal

Clinical ChemistryAmerican Association for Clinical Chemistry

Published: Feb 1, 1994

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