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We found that about half of the neonate pups subjected to inflammatory insult showed a significant increase in expression of the pore-forming \u03b1<jats:sub>1C<\/jats:sub>-subunit of Ca<jats:sub> v<\/jats:sub> 1.2b channels in adult life. These were the same rats in whom Vip mRNA increased in the colon muscularis externae. Additional experiments showed reduced interaction of histone deacetylase (HDAC) 3 with \u03b1<jats:sub> 1C<\/jats:sub> 1b promoter that increased the acetylation of histone H3 lysine 9 (H3K9) in the core promoter region. Vasoactive intestinal peptide (VIP) treatment of na\u00efve muscularis externae swiftly recruited CREB-binding protein (CBP) to the \u03b1<jats:sub> 1C<\/jats:sub> 1b promoter and dissociated HDAC3 from this region to initiate transcription. The CBP interaction with the \u03b1<jats:sub> 1C<\/jats:sub> 1b promoter was transient, but the dissociation of HDAC3 persisted to sustain H3K9 hyperacetylation and increase in transcription. Intraperitoneal treatment of adult na\u00efve rats with butyrate mimicked the effects of neonatal colon inflammation. We concluded that neonatal inflammation upregulates VIP in the colon muscularis externae, which modulates epigenetic events at the \u03b1<jats:sub> 1C<\/jats:sub> 1b promoter to activate \u03b1<jats:sub> 1C<\/jats:sub> 1b gene transcription. Inflammatory insult in early life may be one of the etiologies of smooth muscle dysfunction in adult life, which contributes to the altered motility function in patients with diarrhea-predominant IBS. <\/jats:p>","DOI":"10.1152\/ajpgi.00160.2013","type":"journal-article","created":{"date-parts":[[2013,7,26]],"date-time":"2013-07-26T07:56:00Z","timestamp":1374825360000},"page":"G503-G512","source":"Crossref","is-referenced-by-count":11,"title":["Developmental origins of colon smooth muscle dysfunction in IBS-like rats"],"prefix":"10.1152","volume":"305","author":[{"given":"Qingjie","family":"Li","sequence":"first","affiliation":[{"name":"Enteric Neuromuscular Disorders and Visceral Pain Center, Division of Gastroenterology, Department of Internal Medicine, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John H.","family":"Winston","sequence":"additional","affiliation":[{"name":"Enteric Neuromuscular Disorders and Visceral Pain Center, Division of Gastroenterology, 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