Inflammatory bowel diseases (IBD) are chronic diseases of the gastrointestinal tract that include ulcerative colitis and Crohn's disease. Ulcerative colitis is characterized as a limited inlammation of the colon, usually beginning in the rectum, spreading continuously. The intestinal inflammation, whether caused by infection or abnormal immune response may lead to structural changes in enteric neurons. Studies in animal models have demonstrated the effect of intestinal inflammation on enteric nervous system, following colitis induction with acidic substances such as 2,4,6-trinitrobenzene sulfonic (TNBS). It has been reported the presence of P2X1-P2X7 purinergic receptors in the enteric nervous system. The P2X7 receptor participates in the regulation of several processes such as cell permeability, apoptosis and cytokine release. A recent study has shown that ulcerative colitis reduces the number of P2X7 immunoreactive neurons in myenteric plexus. This project aims to evaluate the effect of Brilliant Blue G (BBG), a P2X7 receptor antagonist, in the enteric nervous system of the large intestine in animals with ulcerative colitis. The distal colon of Wistar rats was submitted to induction of ulcerative colitis by TNBS administration in the large intestine. Treatment with BBG was given 1 hour after induction of colitis and for 5 consecutive days, distal colons are collected 24 hours and 7 days after colitis induction. The animals was divided in control group (not manipulated), Sham 24 h and 7 days (induction was done with vehicle), Colitis 24h, BBG 24h, Colitis 7 days and BBG 7 days. The chemical code, neuronal density and area of enteric neurons reactive to neuronal nitric oxide synthase (NOS, choline acetyl transferase (ChAT) and the P2X7 receptor. The distal colon was analyzed through immunohistochemical techniques for double labelling as the immunoreactivity to P2X7, ChAT and NOS. Histological analysis using staining for Hematoxylin and Eosin was done to evaluate the integrity of the intestinal wall. The results showed a decrease in neurons positive to NOS, ChAT and P2X7 receptor in colitis groups and recovery in neuronal density in the groups treated with BBG. The neural profile area showed an increase in the profile area in the colitis groups and recovery in the groups treated with BBG. In conclusion, BBG was effective in experimental ulcerative colitis and the P2X7 receptor may be a therapeutic target.