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      Chronic administration of fluoxetine and pro-inflammatory cytokine change in a rat model of depression

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          Abstract

          This study evaluated the chronic effects of fluoxetine, a commonly prescribed SSRI antidepressant, on the peripheral and central levels of inflammatory cytokines including IL-1β, IL-6, TNF-α and IL-17 over a 4-interval in a rat model of chronic mild stress (CMS) which resembles the human experience of depression. Twenty-four Sprague-Dawley rats were randomly assigned to CMS+vehicle (n = 9), CMS+fluoxetine (n = 9) and the control (n = 6) groups. Sucrose preference and forced swim tests were performed to assess behavioral change. Blood samples were collected on day 0, 60, 90 and 120 for measurement of cytokine levels in plasma. On day 120, the brain was harvested and central level of cytokines was tested using Luminex. Four months of fluoxetine treatment resulted in changes in the sucrose preference and immobility time measurements, commensurate with antidepressant effects. The CMS+vehicle group exhibited elevated plasma levels of IL-1β, IL-17, and TNF-α on day 60 or 120. Rats treated with fluoxetine demonstrated lower IL-1β in plasma and brain after 90 and 120-day treatment respectively ( p<0.05). There was a trend of reduction of IL-6 and TNF-α concentration. This study revealed the potential therapeutic effects of fluoxetine by reducing central and peripheral levels of IL-1β in the alleviation of depressive symptoms.

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          Most cited references 37

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          Behavioural despair in rats: a new model sensitive to antidepressant treatments.

          Rats when forced to swim in a cylinder from which they cannot escape will, after an initial period of vigorous activity, adopt a characteristic immobile posture which can be readily identified. Immobility was reduced by various clinically effective antidepressant drugs at doses which otherwise decreased spontaneous motor activity in an open field. Antidepressants could thus be distinguished from psychostimulants which decreased immobility at doses which increased general activity. Anxiolytic compounds did not affect immobility whereas major tranquilisers enhanced it. Immobility was also reduced by electroconvulsive shock, REM sleep deprivation and "enrichment" of the environment. It was concluded that immobility reflects a state of lowered mood in the rat which is selectively sensitive to antidepressant treatments. Positive findings with atypical antidepressant drugs such as iprindole and mianserin suggest that the method may be capable of discovering new antidepressants hitherto undetectable with classical pharmacological tests.
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            Validity, reliability and utility of the chronic mild stress model of depression: a 10-year review and evaluation.

             Paul Willner (1997)
            This paper evaluates the validity, reliability and utility of the chronic mild stress (CMS) model of depression. In the CMS model, rats or mice are exposed sequentially, over a period of weeks, to a variety of mild stressors, and the measure most commonly used to track the effects is a decrease in consumption of a palatable sweet solution. The model has good predictive validity (behavioural changes are reversed by chronic treatment with a wide variety of antidepressants), face validity (almost all demonstrable symptoms of depression have been demonstrated), and construct validity (CMS causes a generalized decrease in responsiveness to rewards, comparable to anhedonia, the core symptom of the melancholic subtype of major depressive disorder). Overall, the CMS procedure appears to be at least as valid as any other animal model of depression. The procedure does, however, have two major drawbacks. One is the practical difficulty of carrying out CMS experiments, which are labour intensive, demanding of space, and of long duration. The other is that, while the procedure operates reliably in many laboratories, it can be difficult to establish, for reasons which remain unclear. However, once established, the CMS model can be used to study problems that are extremely difficult to address by other means.
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              Chronic mild stress-induced anhedonia: a realistic animal model of depression.

              Chronic sequential administration of a variety of mild stressors causes a decrease in responsiveness to rewards in rats, which is reversed by chronic administration of antidepressant drugs. This paper reviews the validity of chronic mild stress-induced anhedonia as an animal model of depression, and the evidence that changes in hedonic responsiveness in this model are mediated by changes in the sensitivity of dopamine D2 receptors in the nucleus accumbens. The review opens with an analysis of the design features of animal models of depression, and ends with a brief account of other animal models of anhedonia.
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                Author and article information

                Contributors
                Role: ConceptualizationRole: Funding acquisitionRole: Project administrationRole: SupervisionRole: Writing – original draftRole: Writing – review & editing
                Role: Project administrationRole: Writing – review & editing
                Role: InvestigationRole: Methodology
                Role: Formal analysisRole: Methodology
                Role: SupervisionRole: Writing – review & editing
                Role: ConceptualizationRole: InvestigationRole: MethodologyRole: SupervisionRole: Writing – review & editing
                Role: ConceptualizationRole: Data curationRole: Formal analysisRole: Project administrationRole: SupervisionRole: Writing – review & editing
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                19 October 2017
                2017
                : 12
                : 10
                Affiliations
                [1 ] Department of Clinical Psychology and Psychiatry/School of Public Health, Zhejiang University College of Medicine, Hangzhou, China
                [2 ] Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
                [3 ] Department of Psychological Medicine, National University Health System, Singapore
                [4 ] Shandong Provincial Key Laboratory of Cerebral Microcirculation, Taishan Medical University, Tai’an, China
                [5 ] Department of Medical Psychology, School of Basic Medical Sciences, Taishan Medical University, Tai’an, China
                [6 ] Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada
                [7 ] Mood Disorders Psychopharmacology Unit, University Health Network, Toronto, Ontario, Canada
                [8 ] Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada
                [9 ] Department of Toxicology and Pharmacology, University of Toronto, Toronto, Ontario, Canada
                Radboud University Medical Centre, NETHERLANDS
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Article
                PONE-D-17-25989
                10.1371/journal.pone.0186700
                5648231
                29049348
                © 2017 Lu et al

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                Page count
                Figures: 4, Tables: 2, Pages: 14
                Product
                Funding
                Funded by: funder-id http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81600018
                Award Recipient :
                Funded by: funder-id http://dx.doi.org/10.13039/501100001352, National University of Singapore;
                Award ID: 519600-X11601
                Award Recipient :
                This project was supported by National Science Funds for Young Scientist (81600018 to YL) provided by the National Natural Science Foundation of China (NSFC) and Joint Research Fund for International Cooperation (519600-X11601 to YL) provided by the National University of Singapore. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
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