Lipopolysaccharide induces delayed FosB/DeltaFosB immunostaining within the mouse extended amygdala, hippocampus and hypothalamus, that parallel the expression of depressive-like behavior
Open accessAbstract
Proinflammatory cytokines induce both sickness behavior and depression, but their respective neurobiological correlates are still poorly understood. The aim of the present study was therefore to identify in mice the neural substrates of sickness and depressive-like behavior induced by lipopolysaccharide (LPS, 830 microg/kg, intraperitoneal). LPS-induced depressive-like behavior was dissociated from LPS-induced sickness by testing mice either at 6 h (at which time sickness was expected to be maximal) or at 24 h post-LPS (at which time sickness was expected to be minimal and not to bias the measurement of depressive-like behavior). Concurrently, the expression of acute and chronic cellular reactivity markers (c-Fos and FosB/DeltaFosB, respectively) was mapped by immunohistochemistry at these two time points. In comparison to saline, LPS decreased motor activity in a new cage at 6 h but not at 24 h. In contrast, the duration of immobility in the tail suspension test was increased at both 6 and 24 h. This dissociation between decreased motor activity and depressive-like behavior was confirmed at 24 h post-LPS in the forced swim test. LPS also decreased sucrose consumption at 24 and 48 h, despite normal food and water consumption by that time. At 24 h post-LPS, LPS-induced depressive-like behavior was associated with a delayed cellular activity (as assessed by FosB/DeltaFosB immunostaining) in specific brain structures, particularly within the extended amygdala, hippocampus and hy…
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After LPS, c-fos expression remained elevated 24 hours post-LPS in most structures of the extended amygdala and several hypothalamic areas, and FosB/ΔFosB was also elevated in the hippocampus.
“However, c-fos expression remained elevated 24 hours post-LPS in most of the structures of the extended amygdala and several hypothalamic areas in which a delayed increase in FosB/ΔFosB immunoreactivity was observed. FosB/ΔFos B was also elevated in the hippocampus.”
From From inflammation to sickness and depression: when the immune system subjugates the brain (2008) · cites this paper as [53]
LPS-treated mice displayed increased immobility in the tail-suspension test and forced-swim test 24 hours after treatment, a time when motor activity had returned to normal.
“Some indication that depression-like behaviour remained after sickness behaviour had resolved came from experiments in which LPS-treated mice displayed increased immobility in the tail-suspension test and in the forced-swim test 24 hours after treatment, a time point when motor activity had returned to normal53 (FIG. 3).”
From From inflammation to sickness and depression: when the immune system subjugates the brain (2008) · cites this paper as [53]
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- Authors
- Frenois, F., Moreau, M., O’Connor, J., Lawson, M., Micon, C., Lestage, J., Kelley, K. W., Dantzer, R., & Castanon, N.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Dantzer, Robert
- Venue
- Psychoneuroendocrinology
- Publisher
- Elsevier BV
- Published
- 2007-06
- Volume
- 32
- Issue
- 5
- Pages
- 516-531
- ISSN
- 0306-4530 (ISSN-L)
- PMC
- PMC1978247
- OpenAlex
- W1982754908
- Cited by
- 438
- References
- 12
- Citations by year
- 2026: 14 · 2025: 19 · 2024: 12 · 2023: 22 · 2022: 23 · 2021: 26 · 2020: 24 · 2019: 22 · 2018: 28 · 2017: 25 · 2016: 31 · 2015: 28 · 2014: 24 · 2013: 33 · 2012: 27
- FWCI
- 6.19
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Psychoneuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Institute of Mental Health (MH-079829, R01MH079829, R01MH071349, R01 MH-71349)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- lipopolysaccharide, depression-like behavior, sickness behavior, FosB/ΔFosB, c-fos, inflammatory cytokines, extended amygdala, hippocampus, hypothalamus, tail suspension test, forced swim test, sucrose intake, neuroinflammation, affective circuits
- MeSH terms
- Amygdala, Animals, Depression, Disease Models, Animal, Exploratory Behavior, Hippocampus, Hypothalamus, Immunohistochemistry, Lipopolysaccharides, Male, Motor Activity, Sick Role, Cytokines, Proto-Oncogene Proteins c-fos, Mice
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