The effect of repeated amitriptyline and desipramine administration on cytokine release in C57BL/6 mice

Kubera, Marta; Holáň, Vladimı́r; Mathison, Ronald; Maes, Michaël

doi:10.1016/s0306-4530(00)00026-3

Cited by 67 publications

(38 citation statements)

References 35 publications

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“…The results obtained corroborate those in the literature, showing an antiinflammatory effect for this drug [4,[29][30][31] . However, independently of the treatment period (7, 14 or 28 days), this effect was not observed after the fourth hour of evaluation.…”

Section: Discussionsupporting

confidence: 82%

Amitriptyline and Acute Inflammation: A Study Using Intravital Microscopy and the Carrageenan-Induced Paw Edema Model

Vismari¹,

Alves²,

Palermo-Neto³

2010

Pharmacology

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Background/Aims: Antidepressants are reported to exhibit antiinflammatory effects. However, mechanisms involved in this action have not been elucidated. Thus, the objectives of the present study were (a) to evaluate the effects of amitriptyline on the acute inflammatory process, and (b) to investigate the participation of α₁-adrenergic receptors and glucocorticoids as possible mechanisms implicated in the amitriptyline action on inflammation. Methods and Results: Single and multiple doses of amitriptyline were administered to rats submitted to the carrageenan-induced paw edema model. The results showed a significant antiedematous reaction to amitriptyline, mainly when administered at each elimination half-life. The next step was to evaluate its effects on leukocyte behavior, using intravital microscopy. Amitriptyline produced a significant effect on leukocyte behavior. To investigate possible mechanisms involved, a glucocorticoid receptor antagonist (RU-486) and an α₁-adrenergic receptor antagonist (prazosin) were used. RU-486 administration lacked the ability to decrease the amitriptyline antiinflammatory effects in the carrageenan-induced paw edema model. Prazosin pretreatment potentiated the amitriptyline antiinflammatory effect without presenting an effect per se. Conclusion: The present study shows the ability of amitriptyline to decrease edema and affect leukocyte behavior in an acute inflammatory process; and, for the first time to our knowledge, we suggest the involvement of α₁-adrenoceptors in the antiinflammatory effects of amitriptyline.

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Section: Discussionsupporting

confidence: 82%

Amitriptyline and Acute Inflammation: A Study Using Intravital Microscopy and the Carrageenan-Induced Paw Edema Model

Vismari¹,

Alves²,

Palermo-Neto³

2010

Pharmacology

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“…146 In rats, CMS induces an increased production of IL-1 and IL-2 by stimulated splenocytes 153 Tricyclics appear to be more effective than SSRIs in attenuating the stimulated production of cytokines induced by LPS in vivo Antidepressant-like effects: 5 weeks of imipramine treatment reverses the effects of CMS on stimulated production of IL-1 and IL-2 in rats 153 Antidepressant treatment induces an increase of in vitro-stimulated production of anti-inflammatory cytokines in healthy humans 154 In vitro stimulation of proinflammatory cytokines production induced by LPS and PHA Antidepressant-like effects: Chronic treatment with citalopram or fluoxetine induces an enhanced stimulated production of IL-10 in mice. 148 Chronic treatment with desipramine induces an increase of stimulated production of IL-10 in chronically stressed and nonstressed animals 155 Cell survival pathway dysfunction Alteration of CREB levels in temporal cortex in major depressed patients. 156 Decrease of CREB phosphorylation in the orbitofrontal cortex of depressed patients…”

Section: Modeling Depression In Rodentsmentioning

confidence: 99%

In search of a depressed mouse: utility of models for studying depression-related behavior in genetically modified mice

2004

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The ability to modify mice genetically has been one of the major breakthroughs in modern medical science affecting every discipline including psychiatry. It is hoped that the application of such technologies will result in the identification of novel targets for the treatment of diseases such as depression and to gain a better understanding of the molecular pathophysiological mechanisms that are regulated by current clinically effective antidepressant medications. The advent of these tools has resulted in the need to adopt, refine and develop mouse-specific models for analyses of depression-like behavior or behavioral patterns modulated by antidepressants. In this review, we will focus on the utility of current models (eg forced swim test, tail suspension test, olfactory bulbectomy, learned helplessness, chronic mild stress, drug-withdrawal-induced anhedonia) and research strategies aimed at investigating novel targets relevant to depression in the mouse. We will focus on key questions that are considered relevant for examining the utility of such models. Further, we describe other avenues of research that may give clues as to whether indeed a genetically modified animal has alterations relevant to clinical depression. We suggest that it is prudent and most appropriate to use convergent tests that draw on different antidepressant-related endophenotypes, and complimentary physiological analyses in order to provide a program of information concerning whether a given phenotype is functionally relevant to depressionrelated pathology.

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“…Similar stimulatory effects were observed by Frick et al [10], but that study was performed on animals without tumor cells after oral administration of fluoxetine for four weeks. In our former studies, we also observed the increase in proliferative activity of splenocytes in response to Con A after two and four weeks of desipramine and one or two weeks of fluoxetine ip administration to C57BL/ 6J mice [18,19].…”

mentioning

confidence: 87%

“…Splenocytes were cultured for 72 h at a concentration of 4 × 10 $ cells/ml in the presence or absence of 2.5 µg/ml of Con A. Proliferation was quantified by means of the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Sigma Aldrich) assay described by us earlier [18] and the absorbance was evaluated after 4 h in an ELISA reader (Bio-Rad, USA) at 570 nm.…”

Section: Proliferative Response Of Splenocytes To Mitogen Stimulationmentioning

confidence: 99%

Inhibitory effect of antidepressants on B16F10 melanoma tumor growth

Grygier

Arteta

Kubera

et al. 2013

Pharmacological Reports

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Abstract:Background: Antidepressant drugs, like fluoxetine, a selective serotonin reuptake inhibitor, desipramine, a nonselective noradrenaline reuptake inhibitor, and mirtazapine, an antagonist of noradrenaline a 2 auto-and heteroreceptors, are widely used for the treatment of depressive symptoms in cancer patients. Since these antidepressants have different activities targeting the immune system, they might also modulate tumor growth in cancer patients. Methods: In the present study, we investigated the effects of administration of antidepressant drugs: fluoxetine, desipramine and mirtazapine on B16F10 melanoma tumor growth. These drugs were administered intraperitoneally (ip) for 17 days after subcutaneous injection of B16F10 melanoma cells to male C57BL/6J mice. Results: Fluoxetine significantly inhibited melanoma solid tumor growth and desipramine tended to decrease this parameter whereas mirtazapine had no effect. Conclusion:The inhibitory effect of fluoxetine on melanoma growth was associated with an increased mitogen-induced T cell proliferation which may at least partly participate in the mechanism of the antitumor effect of this antidepressant. It appears that the inhibitory effect of fluoxetine on tumor growth is not related with changes in cytokine levels except for IL-10.

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The effect of repeated amitriptyline and desipramine administration on cytokine release in C57BL/6 mice

Cited by 67 publications

References 35 publications

Amitriptyline and Acute Inflammation: A Study Using Intravital Microscopy and the Carrageenan-Induced Paw Edema Model

Amitriptyline and Acute Inflammation: A Study Using Intravital Microscopy and the Carrageenan-Induced Paw Edema Model

In search of a depressed mouse: utility of models for studying depression-related behavior in genetically modified mice

Inhibitory effect of antidepressants on B16F10 melanoma tumor growth

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