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Impaired parasympathetic function increases susceptibility to inflammatory bowel disease in a mouse model of depression
Open accessAbstract
Clinical and experimental evidence indicates that intestinal inflammatory conditions can be exacerbated by behavioral conditions such as depression. The recent demonstration of a tonic counterinflammatory influence mediated by the vagus nerve in experimental colitis provides a potential link between behavior and gut inflammation. Here we show that experimental conditions that induced depressive-like behaviors in mice increased susceptibility to intestinal inflammation by interfering with the tonic vagal inhibition of proinflammatory macrophages and that tricyclic antidepressants restored vagal function and reduced intestinal inflammation. These results show that reserpine-induced monoamine depletion and maternal separation, 2 models for depression, produced a vulnerability to colitis by a mechanism involving parasympathetic transmission and the presence of gut macrophages. The tricyclic antidepressant desmethylimipramine protected against this vulnerability by a vagal-dependent mechanism. Together these results illustrate the critical role of the vagus in both the vulnerability to inflammation induced by depressive-like conditions and the protection afforded by tricyclic antidepressants and rationalize a clinical evaluation of both parasympathomimetics and tricyclic antidepressants in treatment of inflammatory bowel disease.
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“Critically, vagus nerve dysfunction could exacerbate this neuroinflammatory pathway [43], [52].”
From The hidden genetic and microbial networks connecting neuropsychiatric and digestive disorders (2025) · cites this paper as [52]
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Cited by
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“Experimental sustained depression in mice is followed by impaired parasympathetic function and increased susceptibility to an experimental colitis that was reduced by desmethylimipramine, by a vagally dependent enhanced parasympathetic function (81).”
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Metadata
- Authors
- Ghia, J.-E., Blennerhassett, P., & Collins, S. M.
- Affiliations
- McMaster University (CA)
- Corresponding author
- Collins, Stephen M.
- Venue
- Journal of Clinical Investigation
- Published
- 2008-05-01
- Volume
- 118
- Issue
- 6
- Pages
- 2209-18
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2350428
- OpenAlex
- W2169338224
- Cited by
- 233
- References
- 0
- Citations by year
- 2026: 2 · 2025: 10 · 2024: 13 · 2023: 14 · 2022: 16 · 2021: 10 · 2020: 13 · 2019: 9 · 2018: 12 · 2017: 10 · 2016: 23 · 2015: 16 · 2014: 15 · 2013: 19 · 2012: 10
- FWCI
- 9.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Institut de France
- McMaster University
- Crohn's and Colitis Foundation
- Crohn's and Colitis Foundation of Canada
- Canadian Association of Gastroenterology
- Topics
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- depression, inflammatory bowel disease, vagus nerve, parasympathetic nervous system, colitis, tricyclic antidepressants, desmethylimipramine, reserpine, maternal separation, monoamine depletion, gut-brain axis, neuroimmune regulation
- MeSH terms
- Animals, Antidepressive Agents, Brain, Colitis, Depressive Disorder, Disease Models, Animal, Female, Macrophages, Male, Mice, Inbred C57BL, Parasympathetic Nervous System, Reserpine, Serotonin, Inflammatory Bowel Diseases, Serotonin Agents, Genetic Predisposition to Disease, Mice
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