G A A b st ra ct s in the FST when compared with the sham group receiving saline and rectal ethanol. TNFα was significantly elevated in colonic tissues and in the hippocampus of colitic mice. Hippocampal iNOS expression was significantly increased after induction of colitis and direct measurement of the nitrite content in the hippocampal homogenates was found significantly elevated in colitic mice. Acute NOS inhibition via administration of either L-NAME (30mg/ kg) or AG (20 or 50mg/kg) decreased the immobility time in colitic groups, while at 10 and 5mg/kg respectively no effects were detected. Moreover, acute treatment with NOS inhibitors decreased hippocampal TNF-α level and nitrite content. Treatment with NOS inhibitors did not have any effect on colitis. Conclusion: The present study suggests that the NO pathway might be involved in the behavioral phenotype displayed in the FST by micewith TNBS-induced colitis and that NOS enzyme inhibition could have an antidepressant effect. Our study underscores the potential inflammatory origin of behavioral despair in experimental colitis via the NO pathway. Identification of the cellular mechanism underlying the role of central NO may lead to novel therapeutic targets in depression-associated to IBD.
