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Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
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Behavioral adaptations in a relapsing mouse model of colitis
Chelsea E Matisz1, Fernando A Vicentini2, Simon A Hirota3
1Canadian Center for Behavioural Neuroscience, Department of Neuroscience, University of Lethbridge, 4401 University Drive West, Lethbridge T1K 3M4, AB, Canada.
Physiology & Behavior
|January 14, 2020
Summary
Chronic gut inflammation in mice led to fewer behavioral deficits than acute inflammation, suggesting an adaptive response. Repeated inflammation cycles may normalize memory and stress-coping, unlike acute inflammatory bowel disease (IBD) models.
Area of Science:
- Neuroscience
- Gastroenterology
- Immunology
Background:
- Inflammatory bowel disease (IBD) involves chronic gut inflammation and is linked to neurological and psychological issues.
- Current animal models often use acute inflammation, not reflecting IBD's chronic, relapsing nature.
- Behavioral consequences of IBD require further investigation in chronic models.
Purpose of the Study:
- To compare behavioral changes in mice with acute versus chronic gut inflammation.
- To investigate effects on digging, memory, and stress-coping strategies.
- To understand if repeated inflammation cycles alter behavioral deficits.
Main Methods:
- Mice were exposed to one (acute) or three (chronic) cycles of dextran sodium sulfate (DSS)-induced colitis.
- Gut pathology and colon length were assessed.
- Behavioral tests included object burying, novel object recognition, object location memory, and forced swim task.
Main Results:
- Both acute and chronic DSS treatments caused similar gut pathology.
- Chronically treated mice had significantly shorter colons, indicating more severe disease.
- Acute treatment caused more behavioral deficits (memory, stress-coping) than chronic treatment, except for object burying.
Conclusions:
- Repeated cycles of gut inflammation may induce adaptive or tolerizing effects on memory and stress-coping.
- Acute inflammation models may overestimate behavioral deficits in IBD.
- Potential mechanisms include normalization of the hypothalamic-pituitary-adrenal axis and neuroinflammation.
