3-B-P-040 〇林 周作^1,2、宮田 佳奈¹、山本 武¹、門脇 真¹ Shusaku Hayashi^1,2, Kana Miyata¹, Takeshi Yamamoto¹, Makoto Kadowaki^{1 1}富山大・和漢医薬学総合研究所・消化管生理学分野、²京都薬科大・薬・薬物治療学分野 ¹Univ. Toyama, ²kyoto Pharmaceut. Univ. 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.