Search for biological correlates of depression and mechanisms of action of antidepressant treatment modalities. Do neuropeptides play a role?

Details

Serval ID
serval:BIB_9A0AE7AC878C
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Search for biological correlates of depression and mechanisms of action of antidepressant treatment modalities. Do neuropeptides play a role?
Journal
Physiology and Behavior
Author(s)
Mathé A.A., Husum H., El Khoury A., Jiménez-Vasquez P., Gruber S.H., Wörtwein G., Nikisch G., Baumann P., Agren H., Andersson W., Södergren A., Angelucci F.
ISSN
0031-9384 (Print)
ISSN-L
0031-9384
Publication state
Published
Issued date
2007
Peer-reviewed
Oui
Volume
92
Number
1-2
Pages
226-231
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
Dysregulation of the monoaminergic systems is likely a sufficient but not a necessary cause of depression. A wealth of data indicates that neuropeptides, e.g., NPY, CRH, somatostatin, tachykinins and CGRP play a role in affective disorders and alcohol use/abuse. This paper focuses on NPY in etiology and pathophysiology of depression. Decreased peptide and mRNA NPY were found in hippocampus of both the genetic, e.g., the FSL strain, and environmental rat models of depression, e.g., chronic mild stress and early life maternal separation paradigms. Rat models of alcoholism also show altered NPY. Furthermore, NPY is also reduced in CSF of depressed patients. Antidepressive treatments tested so far (lithium, topiramate, SSRIs, ECT and ECS, wheel running) increase NPY selectively in rat hippocampus and in human CSF. Moreover, NPY given icv to rat has antidepressive effects which are antagonized by NPY-Y1 blockers. The data support our hypothesis that the NPY system dysregulation constitutes one of the biological underpinnings of depression and that one common mechanism of action of antidepressive treatment modalities may be effects on NPY and its receptors. In a novel paradigm, early life maternal separation was superimposed on "depressed" FSL and control rats and behavioral and brain neurochemistry changes observed in adulthood. The consequences were more deleterious in genetically vulnerable FSL. Early antidepressive treatment modulated the adult sequelae. Consequently, if these data are confirmed, the ethical and medical question that will be asked is whether it is permissible and advisable to consider prophylactically treating persons at risk.
Keywords
Animals, Antidepressive Agents/therapeutic use, Depressive Disorder/cerebrospinal fluid, Depressive Disorder/drug therapy, Disease Models, Animal, Electroconvulsive Therapy, Fructose/analogs &amp, derivatives, Fructose/therapeutic use, Hippocampus/drug effects, Hippocampus/metabolism, Humans, Lithium Compounds/therapeutic use, Maternal Deprivation, Neuropeptide Y/cerebrospinal fluid, Neuropeptide Y/genetics, RNA, Messenger/analysis, Rats, Rats, Inbred Strains, Serotonin Uptake Inhibitors/therapeutic use, Social Environment
Pubmed
Web of science
Create date
10/03/2008 10:37
Last modification date
20/08/2019 15:01
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