ArticlePsychopharmacology2009
The type 1 TNF receptor and its associated adapter protein, FAN, are required for TNFalpha-induced sickness behavior.
Article in Psychopharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 40 citations in OpenAlex.
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- Visceral Inflammation and Immune Activation Stress the Brain.Frontiers in immunology · 2017Review
- PKR deficiency alters E. coli-induced sickness behaviors but does not exacerbate neuroimmune responses or bacterial load.Journal of neuroinflammation · 2015Article
- Neuroinflammation and comorbidity of pain and depression.Pharmacological reviews · 2014Review
- The inflammasome: pathways linking psychological stress, depression, and systemic illnesses.Brain, behavior, and immunity · 2013Review
- Differential roles of TNFR1 and TNFR2 signaling in adult hippocampal neurogenesis.Brain, behavior, and immunity · 2013Article
- Immune-neural connections: how the immune system's response to infectious agents influences behavior.The Journal of experimental biology · 2013Review
- Toll-like receptor signaling in neural plasticity and disease.Trends in neurosciences · 2011Review
- Lack of aggression and anxiolytic-like behavior in TNF receptor (TNF-R1 and TNF-R2) deficient mice.Brain, behavior, and immunity · 2010Article
- Central administration of lipopolysaccharide induces depressive-like behavior in vivo and activates brain indoleamine 2,3 dioxygenase in murine organotypic hippocampal slice cultures.Journal of neuroinflammation · 2010Article
- Article
- Serum levels of soluble TNF-α receptors but not BDNF are associated with apathy symptoms in mild Alzheimer's disease and amnestic mild cognitive impairment.Dementia & neuropsychologiaArticle
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
rationaleDuring the course of an infection, the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) acts in the brain to trigger development of behavioral responses, collectively termed sickness behavior. Biological activities of TNFalpha can be mediated by TNF receptor type 1 (TNF-R1) and type 2 (TNF-R2). TNFalpha activates neutral sphingomyelinase through the TNF-R1 adapter protein FAN (factor associated with neutral sphingomyelinase activation), but a behavioral role of FAN in the brain has never been reported.
objectivesWe hypothesized that TNFalpha-induced sickness behavior requires TNF-R1 and that FAN is a necessary component for this response. MATERIALS AND
methodsWe determined the role of brain TNF-R1 in sickness behavior by administering an optimal amount of TNFalpha intracerebroventricularly (i.c.v., 50 ng/mouse) to wild-type (WT), TNF-R1-, TNF-R2-, and FAN-deficient mice. Sickness was assessed by decreased social exploration of a novel juvenile, induction of immobility, and loss of body weight.
resultsTNF-R1-deficient mice were resistant to the sickness-inducing properties of i.c.v. TNFalpha, whereas both TNF-R2-deficient and WT mice were fully responsive. Furthermore, the complete absence of TNFalpha-induced sickness behavior in FAN-deficient mice provided in vivo evidence that FAN-dependent TNF-R1 signaling is critical for this central action of TNFalpha.
conclusionsThis is the first report to demonstrate that TNFalpha-induced sickness behavior is fully mediated by TNF-R1 and that the adaptor protein FAN is a necessary intracellular intermediate for sickness behavior.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.