Abstract <p>Investigation of molecular mechanisms behind interoceptionof pain signals remains one of the most pressing issues in visceralphysiology. Chronic abdominal pain is one of the types of pain sensitivity, whicharises from gastrointestinal tract disorders and often persistsafter their resolution. The development of abdominal pain syndromeis triggered by molecular alterations in the intestinal wall, the detailsof which remain unexplored. TRPV1 and TRPA1 are transient receptorpotential family channels located in the neurons of the entericnervous system and involved in the perception of visceral pain and hypersensitivity.The rat colon exhibits an uneven distribution of these channelsalong its proximal–distal axis. It is hypothesized that these channelsmay be implicated in the initial stages of abdominal pain sensitivityformation. The aim of this study was to investigate colonic segment-specificchanges in the levels of TRPV1 and TRPA1 channels following theinitiation of intestinal inflammation by a single lipopolysaccharide(LPS) administration. The study employed the hot and cold plate(HCP) test for pain sensitivity, morphometric analysis, electrophysiologicalrecordings in the Ussing chamber, and Western blotting to assessTRPA1 and TRPV1 protein levels. A single LPS administration ledto a decrease in TRPA1 levels in both the ascending and descendingcolon. No changes in TRPV1 levels were observed in the ascendingcolon, while a significant increase in TRPV1 levels was recordedin the descending colon. The HCP test revealed no changes in nociception.Thus, in a direct LPS-induced toxicity model, colonic segment-specificchanges in TRPV1 and TRPA1 levels were identified.</p>