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Articles in PresS, published online ahead of print August 28, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00314.2002
Submitted on July 29, 2002
Accepted on August 22, 2002
1 Department of Intestinal Disease Research Program, McMaster University, Hamilton, Ontario, Canada; Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
2 Department of Psychiatry, McMaster University, Hamilton, Ontario, Canada
* To whom correspondence should be addressed. E-mail: perdue{at}mcmaster.ca.
Intestinal dysfunction is related to stress and early life events, but the mechanisms are largely unknown. Our aim was to determine if early trauma predisposes adult rats to intestinal mucosal dysfunction in response to stress. Neonatal Sprague-Dawley rats were individually separated from their mothers for 3 h/day at 4-21 days of age. Between days 80-90, separated and control rats were subjected to mild acute stress (30 min water avoidance) or sham stress.
Mucosal barrier function and ion transport were assessed in colonic tissues mounted in Ussing chambers. Mild stress increased short-circuit current, conductance and transepithelial transport of macromolecules in separated rats, while having minimal effects in controls. Pretreatment
of the separated rats with a corticotropin-releasing hormone (CRH) antagonist, the peptide 
-helical CRH (9-41) injected i.p. 20 min prior to stress, abolished the stress-induced mucosal changes. Our results indicate that neonatal trauma can induce phenotypic changes in adulthood, including enhanced vulnerability of the gut mucosa to stress via mechanisms involving peripherally located CRH receptors.
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