EFEITO DA COLITE ULCERATIVA EXPERIMENTAL SOBRE O RECEPTOR P2X7 NO SISTEMA NERVOSO ENTÉRICO DE

DA SILVA, M. V. Effect of experimental ulcerative colitis on the P2X7 receptor in the enteric nervous system of rats. 2011 135 P (Master Thesis) Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, 2011. The digestive tract the ulcerative colitis and Crohn's disease presents as process intestinal necrosis pathophysiological. This project aimed to study receptor P2X7 and chemical code of the distal colon in enteric nervous system of rat undergoing experimental Ulcerative Colitis. The chemical code, area and neuronal density were analyzed in the enteric neurons immunoreactive for nitric oxide synthase (NOS), choline acetyl transferase (ChAT), Calbindin, calretinin and glial cells (S100) with P2X7 receptor. The analyzed was done in the distal colon of rats: a) Ulcerative Colitis with TNBS aDMinistration (2, 4, 6trinitrobenzene sulfonic acid) (colitis group) b) sham rats injected with PBS and c) animals with no intervention (control group). Tissues were prepared for immunohistochemical double staining methods P2X7 receptor, ChAT, Calbindin, Calretinin, anti-HuC/D and S100. Colocalization the enteric nervous system of the P2X7 receptor-ir (immunoreactive)ir, with NOS-ir neurons, ChAT-ir, Calbindin-ir, Calretinin-ir, HuC/D-ir and S100-ir cells in the control, PBS and Colitis groups. The colitis group neurons showed deformed the NOS-IR neurons in the myenteric plexus. The decrease the colocalization of P2X7 receptor neurons NOS-ir (4.7%), ChAT-ir (9.7%), Calbindin-ir (10%), Calretinin-ir (3.4%), HuC/Dir neurons (6.8%) and S100 (9.5%) in the myenteric plexus. In the submucosal plexus the Calbindin-ir neurons increased by 6%, Calretinin-ir neurons increase of 13.5% and antiHuC/D-ir 18.5% reduction in the Colitis group. There were morphological changes such as increased neutrophils, disintegration of the intestinal epithelium and goblet cells and decreased of collagen. The neuronal density decreased in the myenteric plexus of 42.28%, 34.9%, 22.87%, 60.57%, 14.69% and 29.2% NOS-ir, ChAT-ir, Calbindin-ir, calretinin-ir, HuC/D-ir neurons and S100-ir cells. In the submucosal plexus were decreased by 34.74%, 11.68%, 33.44% and 44.20% Calbindin-ir, Calretinin-ir, HuC/D-ir neurons and glial cells S100-ir, respectively, in the Colitis group. The profile area were reduced by 6.8% and 21% NOS-ir and ChAT-ir neurons, respectively, there was increase 20% of Calbindin-ir neurons. There was decrease in the submucosal plexus profil e area, maximum and minimum diameters in the Calbindin-ir neurons, no change in the parameters by Calretinin-ir neurons. This study demonstrated that colitis affect the enteric nervous system neurons with their respective chemical codes that can cause changes in morphology and motility.