Differential effect of chronic antidepressant treatments on lipopolysaccharide-induced depressive-like behavioural symptoms in the rat

Yan, Shi; Connor, Thomas J.; Nolan, Yvonne M.; Kelly, John; Leonard, Brian E.

doi:10.1016/s0024-3205(99)00430-0

Cited by 117 publications

(82 citation statements)

References 34 publications

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“…A similar attenuation of LPS-induced sickness behavior has been recently reported following chronic administration of the TCA desipramine, but not the SSRI paroxetine or the selective norepinephrine reuptake inhibitor venlafaxine (Shen et al 1999). The results of the present study indicate that chronic treatment with the SSRI fluoxetine can attenuate LPS-induced anorexia and body-weight loss.…”

Section: Discussionsupporting

confidence: 90%

“…5 Fluoxetine Attenuates Sickness Behavior 541 ing alterations in monoaminergic systems (e.g., secretion of norepinephrine and serotonin) and CRH levels, which are considered as the main targets for antidepressants' therapeutic actions. With respect to their effects on behavioral parameters, the fact that TCAs seem to be superior to SSRIs (Shen et al 1999;Yirmiya 1996, and the results of the present study) suggests that antidepressant-induced changes in the noradrenergic system may be more important. However, the lack of information on the neurochemistry of LPS-induced sickness behavior does not allow speculation on the specific role of each monoamine.…”

supporting

confidence: 50%

“…Similar findings were recently reported using chronic treatment with the TCA desipramine. However, in that study, treatment with paroxetine and venlafaxine (selective reuptake inhibitors of serotonin and norepinephrine, respectively) did not attenuate LPS-induced sickness behavior (Shen et al 1999). One aim of the present study was to extend these findings by examining the effects of the SSRI fluoxetine (Prozac) on LPS-induced sickness behavior.…”

mentioning

confidence: 65%

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Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Yirmiya

Pollak

Barak

et al. 2001

Neuropsychopharmacology

203

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Antidepressants produce various immunomodulatory effects, as well as an attenuation of the behavioral responses to immune challenges, such as lipopolysaccharide (LPS). To explore further the effects of antidepressants on neuroimmune interactions, rats were treated daily with either fluoxetine (Prozac) or saline for 5 weeks, and various behavioral, neuroendocrine, and immune functions were measured following administration of either LPS or saline. Chronic fluoxetine treatment significantly attenuated the anorexia and body weight loss, as well as the depletion of CRH-41 from the median eminence and the elevation in serum corticosterone levels induced by LPS. Chronic treatment with imipramine also attenuated LPS-induced adrenocortical activation. In rats and in mice, which normally display a biphasic body temperature response to LPS (initial hypothermia followed by hyperthermia), chronic treatment with fluoxetine completely abolished the hypothermic response and facilitated and strengthened the hyperthermic response. The effects of antidepressants on the responsiveness to LPS are probably not mediated by their effects on peripheral proinflammatory cytokine production, because LPS-induced expression of TNFSeveral lines of evidence indicate that antidepressants produce various immunomodulatory effects. In depressed patients, the effects of antidepressants are variable and seem to be related to the immune status of the patients at the initiation of the treatment. When depression was associated with immune activation, antidepressants reduced immune function and cytokine secretion. For example, the increased plasma levels of IL-6 during acute depression were normalized by 8-week treatment with fluoxetine (Sluzewska et al. 1995), the increased monocyte counts in depressed patients were reduced following 6-weeks treatment with tricyclic antidepressants (TCAs) (Seidel et al. 1996), and the increased numbers of leukocytes and neutrophils were also reduced by antidepressant treatment (Maes et al. 24 , NO . 5 1997). On the other hand, when immune functions were found to be normal, antidepressants had no immunological effects; for example, chronic moclobemide treatment had no effect on monocytes functions, TNF ␣ production or IFN ␥ levels (Landmann et al. 1997). Moreover, in a study of depressed patients who exhibited immune suppression before treatment, the TCA clomipramine increased the production of IL-1 ␤ , IL-2, and IL-3 (Weizman et al. 1994).In experimental animals, TCAs as well as selective serotonin reuptake inhibitors (SSRIs) produce mainly immune suppression and anti-inflammatory effects. For example, antidepressant treatment in vivo inhibited the increased acute phase response in olfactory bulbectomized rats, a useful animal model of depression (Song and Leonard 1994), reduced the production of interleukin-1 (IL-1) and IL-2 in a chronic mild stress model of depression (Kubera et al. 1996), inhibited immune activation in rats with experimental allergic neuritis (Zhu et al. 1994), and produced anti-inflammatory ...

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Section: Discussionsupporting

confidence: 90%

supporting

confidence: 50%

mentioning

confidence: 65%

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Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Yirmiya

Pollak

Barak

et al. 2001

Neuropsychopharmacology

203

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“…The delayed establishment of this long-term depressive-like behavior probably reflects the time required for the cytokine-induced neurobiochemical changes underlying depressive-like symptoms to fully develop. Moreover, it is important to note that our experimental paradigm allowed mice free access to food and water before and during the test, which increased the probability that intake of the highly palatable sucrose solution was mostly based on its rewarding properties (De La Garza, 2005;Merali et al, 2003;Shen et al, 1999). All these data point therefore to the ability of BCG to induce chronic depressive-like behavior, independently of its sickness inducing properties.…”

Section: Discussionmentioning

confidence: 92%

“…Instead of being based on its sensitivity to antidepressant drugs, this animal test of depression directly models a core symptom of depression, namely anhedonia, i.e. the lack of interest in pleasurable activities including consumption of palatable foods (Monleon et al, 1995;Shen et al, 1999). Interestingly, BCG still reduced sucrose intake 3 weeks after inoculation, whereas food and water consumption were normalized by the end of the first week (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Inoculation of Bacillus Calmette-Guerin to mice induces an acute episode of sickness behavior followed by chronic depressive-like behavior

Moreau

André

O’Connor

et al. 2008

Brain, Behavior, and Immunity

142

151

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Although cytokine-induced sickness behavior is now well-established, the mechanisms by which chronic inflammation and depression are linked still remain elusive. Therefore this study aimed to develop a suitable model to identify the neurobiological basis of depressive-like behavior induced by chronic inflammation, independently of sickness behavior. We chose to measure the behavioral consequences of chronic inoculation of mice with Bacillus Calmette-Guerin (BCG), which has been shown to chronically activate both lung and brain indoleamine 2,3-dioxygenase (IDO), a tryptophan-catabolizing enzyme that mediates the occurrence of depressive-like behavior following acute innate immune system activation. BCG inoculation induced an acute episode of sickness (approximately 5 days) that was followed by development of delayed depressive-like behaviors lasting over several weeks. Transient body weight loss, reduction of motor activity and the febrile response to BCG were dissociated temporarily from a sustained increase in the duration of immobility in both forced swim and tail suspension tests, reduced voluntary wheel running and decreased preference for sucrose (a test of anhedonia). Moreover, we show that a distinct pattern of cytokine production and IDO activation parallels the transition from sickness to depression. Protracted depressive-like behavior, but not sickness behavior, was associated with sustained increase in plasma interferon-γ and TNF-α concentrations and peripheral IDO activation. Together, these promising new data establish BCG inoculation of mice as a reliable rodent model of chronic inflammation-induced depressive-like behaviors that recapitulate many clinical observations and provide important clues about the neurobiological basis through which cytokines may have an impact on affective behaviors.

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Inflammation in the Pathogenesis of Depression

Connor¹,

Harkin²

2014

Neuroinflammation and CNS Disorders

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Differential effect of chronic antidepressant treatments on lipopolysaccharide-induced depressive-like behavioural symptoms in the rat

Cited by 117 publications

References 34 publications

Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Inoculation of Bacillus Calmette-Guerin to mice induces an acute episode of sickness behavior followed by chronic depressive-like behavior

Inflammation in the Pathogenesis of Depression

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