Depressive-like behavior induced by tumor necrosis factor-α in mice

Kaster, Manuella P.; Gadotti, Vinícius M.; Calixto, João B.; Santos, Adair R.S.; Rodrigues, Ana Lúcia S.

doi:10.1016/j.neuropharm.2011.08.018

Cited by 257 publications

(132 citation statements)

References 61 publications

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“…For example, central administration of TNFα induced depression-like behaviors in the forced swimming test and tail suspension test (Kaster et al, 2012), while treatment with the TNFα inhibitor infliximab and targeted deletion of TNF receptors had antidepressant effects in mice (Simen et al, 2006;Karson et al, 2013). In agreement with previous studies, we found that administration of TNFα inhibitors reduced by ~20~30% the number of mice that developed learned helplessness, suggesting that stress-induced TNFα contributes to learned helplessness.…”

Section: Discussionsupporting

confidence: 91%

“…Administration of TNFα inhibitors tended to reduce the number of mice that developed learned helplessness, as 45% of the TNFα inhibitor-treated mice and 55% of the etanercepttreated mice exhibited learned helplessness ( Figure 9A). This supports previous reports that inhibiting TNFα exerts antidepressant properties in mouse models of depression (Karson et al, 2013;Simen et al, 2006: Kaster et al, 2012, but also demonstrates that inhibiting TNFα only modestly reduces the induction of learned helplessness depression-like behavior.…”

Section: Tlr4 −/− Mice Display Resistance To Learned Helplessness Depsupporting

confidence: 91%

“…Since hippocampal TNFα was increased after stress, many studies have linked TNFα to depression (Dantzer and Kelley 2007;Palin et al, 2008;Tonelli et al, 2008;Dean, 2011;Kaster et al, 2012;Pandey et al, 2012), and TNFα production was blocked by the antidepressant fluoxetine, we tested if blocking TNFα is sufficient to provide resistance to learned helplessness. TNFα was inhibited using either a newly developed small molecule TNFα inhibitor, Vax-ATC1, or the classical TNFα antagonist etanercept.…”

Section: Tlr4 −/− Mice Display Resistance To Learned Helplessness Depmentioning

confidence: 99%

See 2 more Smart Citations

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Cheng

Jope

Beurel

2016

Psychoneuroendocrinology

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Section: Discussionsupporting

confidence: 91%

Section: Tlr4 −/− Mice Display Resistance To Learned Helplessness Depsupporting

confidence: 91%

Section: Tlr4 −/− Mice Display Resistance To Learned Helplessness Depmentioning

confidence: 99%

See 1 more Smart Citation

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Cheng

Jope

Beurel

2016

Psychoneuroendocrinology

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“…Tumor necrosis factor (TNF)-a has an important role in the development and progression of cognitive decline, as well as depressive and anxiety disorders (Bai et al, 2013;Baune et al, 2012;Camara et al, 2013;Kaster et al, 2012). Indeed, peripheral inflammatory conditions like rheumatoid arthritis (RA) and psoriasis that show high levels of circulating TNF-a are associated with psychiatric symptoms, such as cognitive decline, anxiety, and depression (Bassukas et al, 2008;Chandarana et al, 1987;Menter et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Effects of Centrally Administered Etanercept on Behavior, Microglia, and Astrocytes in Mice Following a Peripheral Immune Challenge

Camara

Corrigan

Jaehne

et al. 2014

Neuropsychopharmacol

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“…Patients with major depression have been found to exhibit all of the vital features of inflammation, including elevation of inflammatory cytokines, acute phase proteins, chemokines, adhesion molecules and inflammatory mediators such as prostaglandins. Repeated administration of IL-1, TNF-a and IL-6 elicits depressive-like behaviour in animals [6][7][8]. The mechanisms contributing to pathogenesis of depression incorporate abnormal neurotransmitter metabolism, altered neuro-endocrine functions and distorted neural plasticity [9,10].…”

mentioning

confidence: 99%

Role of Aspirin and Dexamethasone against Experimentally Induced Depression in Rats

Bhatt

Shukla

Raval

et al. 2016

Basic Clin Pharma Tox

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A large number of current studies indicate that inflammatory mediators may contribute to depression in experimental models as well as in human beings. Nevertheless, the subject, whether anti-inflammatory treatments can prevent depression still remains controversial. In the present study, a chronic mild stress (CMS) model of male Sprague Dawley rats was used to investigate the role of anti-inflammatory drugs in the treatment of depression. All the animals in different groups, except the normal control group, were exposed to CMS procedure for 28 days and concurrently treated with aspirin (10 mg/kg, p.o.), dexamethasone (1 mg/kg p.o.) and amitriptyline (10 mg/kg p.o., reference standard), respectively. Amitriptyline was also used in combination with aspirin and dexamethasone to inspect any synergistic effects. Tests performed towards the end of the study included sucrose preference test, behavioural tests like forced swim test, elevated plus-maze, light/dark box, locomotor activity and biochemical estimations like serum cortisol and brain neurotransmitters. Disease control group (CMS-treated) produced significant depressive behaviour in rats. The animals treated with aspirin showed increased sucrose preference, decreased immobility time in forced swim test, decreased serum cortisol and increased brain serotonin levels signifying antidepressant action. In contrast, there was aggravation of depressive behaviour in rats treated with dexamethasone. Together, these findings suggest that aspirin can serve as a potential antidepressant both individually and as adjunctive agent in the treatment of depression. Inhibition of the inflammatory mediators during stress procedures or any other potential physiological and biochemical mechanisms may be involved in its antidepressant effect.Major depression is one of the most commonly diagnosed neuropsychiatric disorders, with a worldwide life-time prevalence of 17%. It is estimated that by 2020, major depression will be the second most disabling condition in the world. Despite considerable strides have been made over the years, treatment-resistant depression (TRD) remains a common condition which accounts for approximately 30% of the depressed population [1,2]. Historically, treatment options for depression and associated disorders have focused on the medications that modify the activity of monoamine neurotransmitter systems [3].Several studies support the role of inflammation and immune system deregulation in pathophysiology of depression [4,5]. Patients with major depression have been found to exhibit all of the vital features of inflammation, including elevation of inflammatory cytokines, acute phase proteins, chemokines, adhesion molecules and inflammatory mediators such as prostaglandins. Repeated administration of IL-1, TNF-a and IL-6 elicits depressive-like behaviour in animals [6][7][8]. The mechanisms contributing to pathogenesis of depression incorporate abnormal neurotransmitter metabolism, altered neuro-endocrine functions and distorted neural plasticity [9,10...

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Depressive-like behavior induced by tumor necrosis factor-α in mice

Cited by 257 publications

References 61 publications

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

Effects of Centrally Administered Etanercept on Behavior, Microglia, and Astrocytes in Mice Following a Peripheral Immune Challenge

Role of Aspirin and Dexamethasone against Experimentally Induced Depression in Rats

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