Inflammatory Bowel Disease (IBD) includes Crohn’s disease and ulcerative colitis (UC), which cause severe inflammation in the gastro-intestinal tract. Symptoms including rectal bleeding, weight loss, and abdominal pain significantly impact patient well-being, leading to stress, anxiety, depression, and can result in severe complications such as infections, cancer, and eventually death. The goal of IBD treatment has evolved from symptom reduction to modifying the disease's course, with various treatments offering personalised approaches. Still, no effective treatment for all cases or a cure are available; all treatments present adverse effects and none of them offer complete effectiveness for all patients. Considering that permeability, motility and nociception are affected in IBD and highly influenced by enteric neurons and considering that voltage-gated sodium (NaV) channels are crucial for neuronal functioning, targeting NaV channels can be potentially beneficial for gastrointestinal disorders. Among all NaV channel subtypes, NaV1.9 is specifically implicated in visceral pain and gut motility and its function can be modulated by inflammatory mediators. As such, NaV1.9 can be a key target for the dysregulated aspects in IBD. In this work, a 3% Dextran Sodium Sulphate (DSS)-induced colitis model was used to mimic human symptoms of UC. Pain assays were established to observe differences in NaV1.9+/+ and NaV1.9-/- strains after DSS treatment, with NaV1.9+/+ demonstrating higher visceral sensitivity than NaV1.9-/-, although not significant. This promising result suggest a potential role for NaV1.9 in pain treatment for UC patients. The pharmaceutical industry could leverage these findings to develop new treatments, benefiting patients.