Endotoxin- or pro-inflammatory cytokine-induced sickness behavior as an animal model of depression: focus on anhedonia
Abstract
In humans, exposure to endotoxins or pro-inflammatory cytokines induces a number of neuropsychological symptoms collectively referred to as 'flu-like syndrome'. The degree of overlap between flu-like syndrome and major depressive disorder is considerable and a close linkage between these has been predicted to arise due to hypersecretion of endogenous pro-inflammatory cytokines and activation of the hypothalamic pituitary adrenal axis. In animals, exposure to pro-inflammatory cytokines or endotoxins induces a 'sickness behavior' syndrome that is analogous to flu-like symptoms observed in human patients. The goal of the current paper is to review evidence implicating endotoxin- or cytokine-induced sickness behavior as an animal model of depression, with an emphasis on reduced consumption of highly palatable substances as a defining feature.
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Inflammatory challenges involving administration of proinflammatory cytokines ILβ or TNFα trigger a constellation of sickness behaviors in rodents including hypersomnia, fatigue, anorexia, impaired cognitive abilities, psychomotor retardation, and reduced social and exploratory behavior.
“inflammatory challenges that involve administration of the proinflammatory cytokines ILβ or TNFα trigger a constellation of several sickness behaviors in rodents that includes hypersomnia, fatigue, anorexia, impaired cognitive abilities, psychomotor retardation, and reduced social and exploratory behavior”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as De La Garza, 2005
Peripheral inflammation induces depressive-like behaviors in animal models, including anhedonia, reduced exploratory, novelty-seeking and social behaviors, reduced food intake, and sleep disturbance.
“Of particular relevance for this review, peripheral inflammation has been shown to induce depressive-like behaviors in animal models, including anhedonia (e.g., reduced sucrose consumption), decreases in exploratory, novelty-seeking and social behaviors, reduced food intake; and sleep disturbance (Anisman and Matheson, 2005; De La Garza, 2005; Dunn et al., 2005; Larson and Dunn, 2001; Pecchi et al”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as De La Garza, 2005
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References 106 · Cited by 153
- Authors
- De La Garza, R.
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 2005-01
- Volume
- 29
- Issue
- 4-5
- Pages
- 761-770
- ISSN
- 0149-7634 (ISSN-L)
- OpenAlex
- W2050053094
- Cited by
- 153
- References
- 106
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 3 · 2021: 11 · 2020: 13 · 2019: 7 · 2018: 10 · 2017: 5 · 2016: 8 · 2015: 6 · 2014: 8 · 2013: 2 · 2012: 6
- FWCI
- 0.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1r03da015126-01)
- National Institute on Drug Abuse (DA 15126-01)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- sickness behavior, endotoxin, inflammatory cytokines, animal models of depression, anhedonia, influenza-like illness, major depressive disorder, hypothalamic-pituitary-adrenal axis, palatable food intake, neuroinflammation
- MeSH terms
- Affect, Animals, Behavior, Animal, Behavioral Symptoms, Depression, Disease Models, Animal, Endotoxins, Humans, Psychoneuroimmunology, Cytokines
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