Lipopolysaccharide-induced anhedonia is abolished in male serotonin transporter knockout rats: An intracranial self-stimulation study

Heesch, Floor van; Prins, Jolanda; Konsman, Jan Pieter; Westphal, Koen G.C.; Olivier, Berend; Kraneveld, Aletta D.; Korte, S. Mechiel

doi:10.1016/j.bbi.2012.12.013

Cited by 41 publications

(26 citation statements)

References 45 publications

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“…These effects are in line with data demonstrating the association between anhedonia and neuroinflammation following the administration of the cytokine inducer lipopolysaccharide [47] suggesting that neuroinflammation is closely associated with the development of the depressive-like behavior, rather than being a consequence of stress exposure. However, further studies are demanded to establish whether the decreased sucrose consumption is a consequence of the inflammatory state or if the latter develops in close association with the behavioral deficit.…”

Section: Discussionsupporting

confidence: 88%

Stress-induced anhedonia is associated with the activation of the inflammatory system in the rat brain: Restorative effect of pharmacological intervention

Rossetti

Papp

Gruca

et al. 2016

Pharmacological Research

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Section: Discussionsupporting

confidence: 88%

Stress-induced anhedonia is associated with the activation of the inflammatory system in the rat brain: Restorative effect of pharmacological intervention

Rossetti

Papp

Gruca

et al. 2016

Pharmacological Research

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“…It should be noted that acute systemic administration of low-dose LPS (~100 μg/kg) has been reported to either decrease tissue DA content or increase extracellular DA metabolites in the NAcc (van Heesch et al, 2014;Yeh et al, 2015). However, these studies assessed DA and 'anhedonic' behavior (sucrose preference or responding for brain stimulation) at 2-4 h post LPS (van Heesch et al, 2014;van Heesch et al, 2013;Yeh et al, 2015), a time point that may be confounded due to the febrile effects of LPS and related sickness behaviors (Dinarello, 2004;Frenois et al, 2007;O'Connor et al, 2009b). These early effects of LPS may also reflect, for instance, acute activation of neuroendocrine peptides and hormones (minutes to hours), which can have stimulatory effects on turnover or release of brain catecholamines (Barrot et al, 2000;Lavicky and Dunn, 1993;Matsuzaki et al, 1989;Mekaouche et al, 1996), and which may occur ahead of the more chronic mechanisms by which inflammation is thought to contribute to decreased DA availability (see the section 'Mechanisms of inflammation effects on dopamine synthesis and release' below for detailed discussion).…”

Section: Biochemical and Behavioral Studies In Laboratory Animalsmentioning

confidence: 97%

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Felger

Treadway

2016

Neuropsychopharmacol

306

237

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Motivational and motor deficits are common in patients with depression and other psychiatric disorders, and are related to symptoms of anhedonia and motor retardation. These deficits in motivation and motor function are associated with alterations in corticostriatal neurocircuitry, which may reflect abnormalities in mesolimbic and mesostriatal dopamine (DA). One pathophysiologic pathway that may drive changes in DAergic corticostriatal circuitry is inflammation. Biomarkers of inflammation such as inflammatory cytokines and acute-phase proteins are reliably elevated in a significant proportion of psychiatric patients. A variety of inflammatory stimuli have been found to preferentially target basal ganglia function to lead to impaired motivation and motor activity. Findings have included inflammation-associated reductions in ventral striatal neural responses to reward anticipation, decreased DA and DA metabolites in cerebrospinal fluid, and decreased availability, and release of striatal DA, all of which correlated with symptoms of reduced motivation and/or motor retardation. Importantly, inflammation-associated symptoms are often difficult to treat, and evidence suggests that inflammation may decrease DA synthesis and availability, thus circumventing the efficacy of standard pharmacotherapies. This review will highlight the impact of administration of inflammatory stimuli on the brain in relation to motivation and motor function. Recent data demonstrating similar relationships between increased inflammation and altered DAergic corticostriatal circuitry and behavior in patients with major depressive disorder will also be presented. Finally, we will discuss the mechanisms by which inflammation affects DA neurotransmission and relevance to novel therapeutic strategies to treat reduced motivation and motor symptoms in patients with high inflammation.

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“…Proinflammatory cytokines increase the expression of SERT via a mitogen-activated protein kinase p38 pathway. Genetic deletion of SERT abrogates the depression-like behavioral effects of LPS, 26,27 although contradictory results concerning the ability of cytokines to stimulate SERT have been reported. 28 …”

Section: Activation Of Ido Induces Depression-like Behavior By a Glutmentioning

confidence: 99%

Is there a role for glutamate-mediated excitotoxicity in inflammation-induced depression?

2014

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Chronic inflammation in physically ill patients is often associated with the development of symptoms of depression. The mechanisms that are responsible for inflammation-associated depression have been elucidated over the last few years. Kynurenine produced from tryptophan in a reaction catabolized by indoleamine 2,3 dioxygenase is transported into the brain where it is metabolized by microglial enzymes into a number of neurotropic compounds including quinolinic acid, an agonist of N-methyl-D-aspartate receptors. Quinolinic acid can synergize with glutamate released by activated microglia. This chain of events opens the possibility to treat inflammation-induced depression using therapies that target the transport of kynurenine through the blood-brain barrier, the production of quinolinic acid and glutamate by activated microglia, or the efflux of glutamate from the brain to the blood.

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Lipopolysaccharide-induced anhedonia is abolished in male serotonin transporter knockout rats: An intracranial self-stimulation study

Cited by 41 publications

References 45 publications

Stress-induced anhedonia is associated with the activation of the inflammatory system in the rat brain: Restorative effect of pharmacological intervention

Stress-induced anhedonia is associated with the activation of the inflammatory system in the rat brain: Restorative effect of pharmacological intervention

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Is there a role for glutamate-mediated excitotoxicity in inflammation-induced depression?

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