We aimed to investigate neurogenesis in the enteric nervous system of murine colons with experimental colitis to elucidate the mechanisms that cause colonic motility disturbances in the colitis. In the motility study, veratridine, a neuroactivator induced TTX-sensitive contractions in the normal murine colons, whereas these contractions were significantly suppressed in colitis murine colons. Immunohistochemical analyses revealed that there were no significant differences in a number of myenteric neurons (pan-neural marker HuC/D-positive neurons) in the colons between normal and colitis mice, whereas the proportion of nitrergic neurons (nNOS-positive) per ganglion was significantly increased in the colons of colitis mice compared to normal mice. Furthermore, the proportion of Sox2 (neural stem cell marker)-positive nitrergic neurons among Sox2-positive neurons per ganglion was significantly increased in the colons of colitis mice compared to normal mice. In addition, L-NAME, a NOS inhibitor significantly enhanced veratridine-induced colonic contractions in colitis mice rather than normal mice. These results suggest that the colitis cause an imbalance in the enteric neural circuit composed of excitatory neurons and inhibitory neurons in the myenteric plexus of the colon, which results in the colonic dysmotility.