The digestive tracts of
ulcerative colitis and
Crohn's disease patients present with pathophysiological processes and intestinal
necrosis. This study examined the
P2X7 receptor and changes in the distal colon in enteric neurons of rats with experimental
ulcerative colitis. The analysis was performed in the distal colons of rats with
ulcerative colitis induced by the administration of
2,4,6-trinitrobenzene sulfonic acid (
colitis group). The survival time after
colitis induction was 24 h. The treated animals were compared to
sham rats injected with
phosphate-buffered saline and to animals with no intervention (control group). Tissues were prepared for immunohistochemical double-staining methods to examine
P2X7 receptor,
choline acetyltransferase (ChAT),
calbindin,
calretinin, anti-HuC/D (pan-neuronal) and S100β (pan-glial). The colocalization of the
P2X7 receptor-immunoreactive (IR) cells was observed in the myenteric plexus with
nitric oxide synthase (NOS)-, ChAT-,
calbindin-,
calretinin- and HuC/D-IR neurons and S100β-IR cells in the control,
sham and
colitis groups. The neuronal density (cell bodies/cm(2)) decreased in the myenteric plexus by 11, 18, 34, 22 and 60% in the
P2X7 receptor, NOS-, ChAT-,
calbindin- and
calretinin-IR neurons, respectively. In addition, the densities (cell bodies/cm(2)) of HuC/D-IR neurons and S100β-IR enteric glial cells decreased by 33 and 29%, respectively. The profile areas were reduced by 6.8 and 21% in NOS- and ChAT-IR neurons, respectively. There was also a 20% increase of
calbindin-IR neurons. Morphological changes were observed, such as increased neutrophils, disintegration of the intestinal epithelium and goblet cells and decreased
collagen. This study demonstrated that
colitis differentially affects
P2X7 receptor-expressing enteric neurons based on their chemical codes and may cause changes in morphology and motility.