Depressive-like behavior induced by tumor necrosis factor-α is attenuated by m-trifluoromethyl-diphenyl diselenide in mice

Brüning, César Augusto; Martini, Franciele; Soares, Suelen Mendonça; Savegnago, Lucielli; Sampaio, Tuane Bazanella; Nogueira, Cristina W.

doi:10.1016/j.jpsychires.2015.04.019

Cited by 40 publications

(14 citation statements)

References 56 publications

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“…Much research has collected substantial evidence from animal studies that support the role of TNF-α in depression [ 48 , 49 , 50 , 51 ]. A study reported in 2012, in which researchers administered TNF-α in animal models, which induced many symptoms such as: decreased social behavior, locomotors activity and anhedonia, suppression of food intake, sleep abnormalities, fatigue, and alterations in cognition.…”

Section: Evidence From Animal and Human Studiesmentioning

confidence: 99%

“…However, knockout of TNF-α receptors in mice increased the levels of 5-HT in the synaptic cleft [ 84 ]. Moreover, a variety of studies have reported that TNF-α could reduce 5-HT availability by activating SERT via trafficking-dependent and independent processes through p38 MAPK activation [ 48 , 50 , 51 , 85 ]. These observation suggested that TNF-α can intensely regulate the the activety of neuronal serotonin transporter.…”

Section: The Pathophysiologic Role Of Tnf-α In Depressionmentioning

confidence: 99%

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Pathogenetic and Therapeutic Applications of Tumor Necrosis Factor-α (TNF-α) in Major Depressive Disorder: A Systematic Review

Zhang

Baloch

2016

IJMS

146

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Major depressive disorder (MDD) is characterized by mood, vegetative, cognitive, and even psychotic symptoms and signs that can cause substantial impairments in quality of life and functioning. Up to now, the exact pathogenesis of MDD remains poorly understood. Recent research has begun to reveal that the pro-inflammatory cytokines, particularly, tumor necrosis factor-α (TNF-α), play an integral role in the pathophysiology of depressive disorders and the mechanism of antidepressant treatment. On the base of several observations: it is found that subsets of MDD patients have enhanced plasma levels TNF-α; antidepressant treatments had linked with the decline of TNF-α; central administration of TNF-α gives rise to sickness behavior which shares features with depression; and a blockade of it can ameliorate depressive symptomatology in animal models and clinical trials. In this review article, we focus on recent evidence linking TNF-α and MDD looking at data from animal and clinical studies, illustrating the pathophysiological role, susceptibility and its therapeutic application in depression. We conclude by discussing future directions for research, in particular the opportunities for the development of novel therapeutics that target TNF-α. This will be very important for designing preventative strategies and for the identification of new drug targets and preventative strategies.

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Section: Evidence From Animal and Human Studiesmentioning

confidence: 99%

Section: The Pathophysiologic Role Of Tnf-α In Depressionmentioning

confidence: 99%

Pathogenetic and Therapeutic Applications of Tumor Necrosis Factor-α (TNF-α) in Major Depressive Disorder: A Systematic Review

Zhang

Baloch

2016

IJMS

146

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“…In addition, the mitogen-activated protein kinase (MAPK) signaling pathway is stimulated by TNF-α, given that inhibition of c-jun N-terminal kinase blocks TNF-α-induced sickness ( 116 ). The MAPK pathway may also be responsible for the effect of TNF-α to induce depression-like behavior at intracerebroventricular (ICV) doses that are too low to induce signs of sickness ( 117 , 118 ).…”

Section: Impact Of Immune Stress Signaling From the Periphery On Braimentioning

confidence: 99%

Visceral Inflammation and Immune Activation Stress the Brain

et al. 2017

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Stress refers to a dynamic process in which the homeostasis of an organism is challenged, the outcome depending on the type, severity, and duration of stressors involved, the stress responses triggered, and the stress resilience of the organism. Importantly, the relationship between stress and the immune system is bidirectional, as not only stressors have an impact on immune function, but alterations in immune function themselves can elicit stress responses. Such bidirectional interactions have been prominently identified to occur in the gastrointestinal tract in which there is a close cross-talk between the gut microbiota and the local immune system, governed by the permeability of the intestinal mucosa. External stressors disturb the homeostasis between microbiota and gut, these disturbances being signaled to the brain via multiple communication pathways constituting the gut–brain axis, ultimately eliciting stress responses and perturbations of brain function. In view of these relationships, the present article sets out to highlight some of the interactions between peripheral immune activation, especially in the visceral system, and brain function, behavior, and stress coping. These issues are exemplified by the way through which the intestinal microbiota as well as microbe-associated molecular patterns including lipopolysaccharide communicate with the immune system and brain, and the mechanisms whereby overt inflammation in the GI tract impacts on emotional-affective behavior, pain sensitivity, and stress coping. The interactions between the peripheral immune system and the brain take place along the gut–brain axis, the major communication pathways of which comprise microbial metabolites, gut hormones, immune mediators, and sensory neurons. Through these signaling systems, several transmitter and neuropeptide systems within the brain are altered under conditions of peripheral immune stress, enabling adaptive processes related to stress coping and resilience to take place. These aspects of the impact of immune stress on molecular and behavioral processes in the brain have a bearing on several disturbances of mental health and highlight novel opportunities of therapeutic intervention.

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“…A previous study has shown that rats subjected to 3‐day intra‐hippocampal or intra‐amygdala IL‐6 treatments manifested a significant increase in the immobility time in the FST (Wu and Lin, 2008). Recent studies also revealed that intracerebroventricular TNF‐α administration produced an increase in immobility time in the FST and in a tail suspension test (Bruning et al, 2015; Kaster et al, 2012). Therefore, our finding regarding IL‐6 mRNA expression levels is in agreement with preclinical data showing a plausible role of pro‐inflammatory cytokine in the pathology of depression‐like behavior induced by PNS by inducing an increased production of pro‐inflammatory cytokines which might trigger neurobiological changes capable of inducing depression.…”

Section: Discussionmentioning

confidence: 99%

Duloxetine prevents the effects of prenatal stress on depressive‐like and anxiety‐like behavior and hippocampal expression of pro‐inflammatory cytokines in adult male offspring rats

Zhang

Wang

et al. 2016

Intl J of Devlp Neuroscience

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Stress during pregnancy may cause neurodevelopmental and psychiatric disorders. However, the mechanisms are largely unknown. Currently, pro-inflammatory cytokines have been identified as a risk factor for depression and anxiety disorder. Unfortunately, there is very little research on the long-term effects of prenatal stress on the neuroinflammatory system of offspring. Moreover, the relationship between antidepressant treatment and cytokines in the central nervous system, especially in the hippocampus, an important emotion modulation center, is unclear. Therefore, the aim of this study was to determine the effects of prenatal chronic mild stress during development on affective-like behaviors and hippocampal cytokines in adult offspring, and to verify whether antidepressant (duloxetine) administration from early adulthood could prevent the harmful consequences. To do so, prenatally stressed and non-stressed Sprague-Dawley rats were treated with either duloxetine (10mg/kg/day) or vehicle from postnatal day 60 for 21days. Adult offspring were divided into four groups: 1) prenatal stress+duloxetine treatment, 2) prenatal stress+vehicle, 3) duloxetine treatment alone, and 4) vehicle alone. Adult offspring were assessed for anxiety-like behavior using the open field test and depression-like behavior using the forced swim test. Brains were analyzed for pro-inflammatory cytokine markers in the hippocampus via real-time PCR. Results demonstrate that prenatal stress-induced anxiety- and depression-like behaviors are associated with an increase in hippocampal inflammatory mediators, and duloxetine administration prevents the increased hippocampal pro-inflammatory cytokine interleukin-6 and anxiety- and depression-like behavior in prenatally stressed adult offspring. This research provides important evidence on the long-term effect of PNS exposure during development in a model of maternal adversity to study the pathogenesis of depression and its therapeutic interventions.

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Depressive-like behavior induced by tumor necrosis factor-α is attenuated by m-trifluoromethyl-diphenyl diselenide in mice

Cited by 40 publications

References 56 publications

Pathogenetic and Therapeutic Applications of Tumor Necrosis Factor-α (TNF-α) in Major Depressive Disorder: A Systematic Review

Pathogenetic and Therapeutic Applications of Tumor Necrosis Factor-α (TNF-α) in Major Depressive Disorder: A Systematic Review

Visceral Inflammation and Immune Activation Stress the Brain

Duloxetine prevents the effects of prenatal stress on depressive‐like and anxiety‐like behavior and hippocampal expression of pro‐inflammatory cytokines in adult male offspring rats

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