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| ROLE OF SEROTONIN IN THE PATHOPHYSIOLOGY OF DEPRESSION - FOCUS ON THE SEROTONIN TRANSPORTER |
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| Author(s): OWENS MJ, NEMEROFF CB |
| Source: CLINICAL CHEMISTRY Volume: 40 Issue: 2 Pages: 288-295 Published: FEB 1994 |
| Times Cited: 415 References: 72 |
| 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; (a) 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 [H-3]imipramine or [H-3]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 or 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. |
| Document Type: Proceedings Paper |
| Language: English |
| Reprint Address: OWENS, MJ (reprint author), EMORY UNIV, SCH MED, DEPT PSYCHIAT & BEHAV SCI, NEUROPSYCHOPHARMACOL, PO DRAWER AF, ATLANTA, GA 30322 USA |
| Publisher: AMER ASSOC CLINICAL CHEMISTRY, 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 |
| Subject Category: Medical Laboratory Technology |
| IDS Number: NA660 |
| ISSN: 0009-9147 |
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