Cited by 100Tryptophan and brain disordersInflammatory Bowel DiseaseStress Responses and Cortisol

Anxiety- and depressive-like behaviors are associated with altered hippocampal energy and inflammatory status in a mouse model of Crohn's disease

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Haj-Mirzaian, Arya, Amiri, Shayan, Amini-Khoei, Hossein, Hosseini, Mir-Jamal, Haj-Mirzaian, Arvin, Momeny, Majid, Rahimi-Balaei, Maryam, Dehpour, Ahmad Reza·2017·Neuroscience

Abstract

Depression and anxiety are common comorbid disorders observed in patients with inflammatory bowel disease (IBD). Increasing line of evidence indicates that immune-inflammatory responses are involved in co-occurrence of mood disorders and IBD. However, the mechanisms through which immune-inflammatory pathways modulate this comorbidity are not yet understood. This study investigated the role of innate immunity in the development of behavioral abnormalities associated with an animal model of Crohn's disease (CD). To do this, we induced colitis in male adult mice by intrarectal (i.r.) injection of DNBS (Dinitrobenzene sulfonic acid). After 3 days, we performed behavioral tests for anxiety- and depressive-like behaviors as well as tissue collection. Our results showed that DNBS-induced colonic inflammatory responses were accompanied by infiltration of inflammatory cells, and increased expression of genes involved in toll-like receptor signaling pathway in intestinal tissue. Furthermore, the DNBS-treated mice showed depressive- and anxiety-like behaviors which were associated with increased expression of the inflammatory genes and abnormal mitochondrial function in the hippocampus. These results suggest that peripheral inflammation is able to increase the transcriptional level of the genes in toll-like receptor pathway, induces abnormal mitochondrial function in the hippocampus, and these negative effects may be involved in the co-occurrence of anxiety and depression in early stages of CD.

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Crossref · 10.1016/j.neuroscience.2017.10.023

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  • Upregulated expression of inflammatory genes and mitochondrial dysfunction in the hippocampus might be responsible for the abnormal behaviors in mice with DNBS-induced colitis.

    “Upregulated expression of inflammatory genes and mitochondrial dysfunction in the hippocampus might be responsible for the abnormal mouse behaviors (70).”
  • Depressive- and anxiety-like behaviors were found in mice with dinitrobenzene sulfonic acid (DNBS)-induced colitis.

    “Depressive- and anxiety-like behaviors were found in mice with dinitrobenzene sulfonic acid (DNBS)-induced colitis.”

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Authors
Haj-Mirzaian, A., Amiri, S., Amini-Khoei, H., Hosseini, M.-J., Haj-Mirzaian, A., Momeny, M., Rahimi-Balaei, M., & Dehpour, A. R.
Affiliations
  • University of Manitoba (CA)
  • Shahrekord University of Medical Sciences (IR)
  • Zanjan University of Medical Sciences (IR)
  • Tehran University of Medical Sciences (IR)
Corresponding author
Dehpour, Ahmad Reza
Venue
Neuroscience
Publisher
Elsevier BV
Published
2017-12
Volume
366
Pages
124-137
ISSN
0306-4522 (ISSN-L)
OpenAlex
W2766723179
Cited by
100
References
128
Citations by year
2026: 4 · 2025: 17 · 2024: 16 · 2023: 17 · 2022: 15 · 2021: 9 · 2020: 7 · 2019: 12 · 2018: 3
FWCI
2.00
Type
journal article
Language
en
Open access
Locations
  • Neuroscience (acceptedVersion)
  • PubMed (publishedVersion)
Funders
Iran National Science Foundation (96002757)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
Crohn's disease, anxiety-like behavior, depression-like behavior, inflammatory bowel disease, comorbid depression and anxiety, mitochondrial dysfunction, Toll-like receptor signaling, peripheral inflammation, DNBS-induced colitis, innate immunity, neuroinflammation
MeSH terms
Animals, Anxiety, Behavior, Animal, Benzenesulfonates, Colitis, Crohn Disease, Depression, Disease Models, Animal, Encephalitis, Hippocampus, Inflammation, Male, Mitochondria, Nitric Oxide

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