We investigated the responses of the hypothalamic-pituitary-adrenal (HPA) axis during experimental
colitis induced by intracolonic administration of 2,4,6-trinitrobenzenesulfonic
acid in the rat. On days 3 and 7 after induction of
colitis, the
corticotropin-releasing hormone (CRH)
mRNA level in the parvocellular paraventricular nucleus (pPVN) of the hypothalamus was reduced, the plasma
ACTH level remained at the basal level, and the plasma
corticosterone (Cort) level was high. Induction of
colitis on day 3 after
adrenalectomy with Cort pellet replacement (ADX + Cort) resulted in a marked increase in CRH
mRNA on day 7 after induction of
colitis compared with noncolitic ADX + Cort animals. Pair feeding to match the food intake of the colitic animals resulted in no significant change in CRH
mRNA in the pPVN, plasma
ACTH, and Cort compared with healthy control animals. These findings indicated that CRH
mRNA expression in the pPVN was inhibited by
glucocorticoid feedback during this experimental
colitis, and the decrease in food intake during
colitis was not simply responsible for the expression of CRH
mRNA. It is inferred that the HPA axis including the CRH level in the pPVN is altered in patients with
inflammatory bowel disease.