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Behavioral Despair Associated With a Mouse Model of Crohn's Disease: Role of Nitric Oxide Pathway Publisher Pubmed



Heydarpour P1, 2 ; Rahimian R1, 3 ; Fakhfouri G3, 4 ; Khoshkish S1, 2 ; Fakhraei N2 ; Salehisadaghiani M1, 2 ; Wang H5 ; Abbasi A6 ; Dehpour AR1, 7 ; Ghia JE5, 8
Authors
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Authors Affiliations
  1. 1. Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, P.O. Box 13145-784, Tehran, Iran
  2. 2. Brain and Spinal Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Psychiatry and Neuroscience, Faculty of Medicine, Laval University, 1050, avenue de la Medecine, Quebec City, QC, Canada
  4. 4. Institut universitaire en sante mentale de Quebec, 2601, Chemin de la Canardiere, Quebec City, QC, Canada
  5. 5. Department of Immunology, University of Manitoba, Winnipeg, MB, Canada
  6. 6. Department of Pathology, Urmia University of Medical Science, Urmia, Iran
  7. 7. Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Department of Internal Medicine section of Gastroenterology, Inflammatory Bowel Disease Clinical and Research Center, University of Manitoba, Winnipeg, MB, Canada

Source: Progress in Neuro-Psychopharmacology and Biological Psychiatry Published:2016


Abstract

Crohn's disease (CD) is associated with increased psychiatric co-morbidities. Nitric oxide (NO) is implicated in inflammation and tissue injury in CD, and it may also play a central role in pathogenesis of the accompanying behavioral despair. This study investigated the role of the NO pathway in behavioral despair associated with a mouse model of CD. Colitis was induced by intrarectal (i.r.) injection of 2,4,6-trinitrobenzenesulfonic acid (10. mg TNBS in 50% ethanol). Forced swimming test (FST), pharmacological studies and tissues collection were performed 72. h following TNBS administration. To address a possible inflammatory origin for the behavioral despair following colitis induction, tumor necrosis factor-alpha (TNF-α) level was measured in both the hippocampal and colonic tissue samples. In parallel, hippocampal inducible nitric oxide synthase (iNOS) and nitrite level were evaluated. Pharmacological studies targeting the NO pathway were performed 30-60. min before behavioral test. Colitis was confirmed by increased colonic TNF-α level and microscopic score. Colitic mice demonstrated a significantly higher immobility time in the FST associated to a significant increase of hippocampal TNF-α, iNOS expression and nitrite content. Acute NOS inhibition using either Nω-nitro-. l-arginine methyl ester (a non-specific NOS inhibitor) or aminoguanidine hydrochloride (a specific iNOS inhibitor) decreased the immobility time in colitic groups. Moreover, acute treatment with both NOS inhibitors decreased the TNF-α level and nitrite content in the hippocampal samples. This study suggests that the NO pathway may be involved in the behavioral effects in the mouse TNBS model of CD. These findings endow new insights into the gut-brain communication during the development of colonic inflammation, which may ultimately lead to improved therapeutic strategies to combat behavior changes associated with gastrointestinal disorders. © 2015 Published by Elsevier Inc.
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